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Six-time Formula One world champion Lewis Hamilton, the first and only Black driver in F1, [...]


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187k

They’re famously known as the Silver Arrows, but for the 2020 season world champions Mercedes will be switching the colours of Lewis Hamilton’s and Valtteri Bottas’s cars to black as they make a stand against racism and discrimination, and pledge to improve the diversity of their team.


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Charles LeClerc and Max Verstappen were among those not to take a knee on the starting grid before the first race of the season


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The Austrian Grand Prix will kick off the new season as Formula 1 returns – get full details on the first eight races here.


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46.1k

Formula 1 has announced the launch of a new F1 Esports Virtual Grand Prix series, featuring a number of current F1 drivers. The series has been created to enable fans to continue watching Formula 1 races virtually, despite the ongoing coronavirus situation.


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Red Bull and AlphaTauri are on the search for a new power unit supplier after Honda made the shock decision to withdraw from Formula 1 at the end of 2021…


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It’s the dawn of a new era for Williams after the Formula 1 team announced they have been acquired by American investment firm Dorilton Capital…


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30.7k
2020-10-26 12:06:00 UTC

Self-awareness check? INTRO MUSIC: Sagittarius V - Lucidator: http://sagittariusvmusic.bandcamp.com DONATE: https://www.subscribestar.com/paul-joseph-watson ...


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28.7k

Charles Leclerc is one of the F1 drivers who has opted against taking a knee before Grands Prix this season.


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27.9k

The Ferrari academy driver, whose father is the legendary seven-time world champion, has been hotly-tipped for a big career in F1 and he will get his first taste of the main event in October.


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Website: bbc.co.uk
2020-11-16 23:35:59 UTC

A group of MPs call on the Prime Minister to recommend Lewis Hamilton for a knighthood after he won a record-equalling seventh F1 world title.


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26k

Sebastian Vettel and Ferrari are set to split at the end of this season after six years together in Formula 1, according to Motorsport-Total sources.


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Four-time world champion Sebastian Vettel will remain in Formula 1 beyond this season after putting pen to paper with Racing Point, which will be rebranded Aston Martin F1 Team from next season…


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Lewis Hamilton says he's


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Sergio Perez talks to F1.com's Lawrence Barretto about interest from Mercedes and Ferrari but ultimately going for McLaren – a decision which shaped his career...


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Mercedes’ Lewis Hamilton has become the most successful driver in terms of victories in Formula 1 history, after a dominant display at the Portuguese Grand Prix saw him claim his 92nd victory from team mate Valtteri Bottas and the Red Bull of Max Verstappen.


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Dogs were the first domesticated animal, likely originating from human-associated wolves, but their origin remains unclear. Bergstrom et al. sequenced 27 ancient dog genomes from multiple locations near to and corresponding in time to comparable human ancient DNA sites (see the Perspective by Pavlidis and Somel). By analyzing these genomes, along with other ancient and modern dog genomes, the authors found that dogs likely arose once from a now-extinct wolf population. They also found that at least five different dog populations ∼10,000 years before the present show replacement in Europe at later dates. Furthermore, some dog population genetics are similar to those of humans, whereas others differ, inferring a complex ancestral history for humanity's best friend. Science , this issue p. [557][1]; see also p. [522][2] Dogs were the first domestic animal, but little is known about their population history and to what extent it was linked to humans. We sequenced 27 ancient dog genomes and found that all dogs share a common ancestry distinct from present-day wolves, with limited gene flow from wolves since domestication but substantial dog-to-wolf gene flow. By 11,000 years ago, at least five major ancestry lineages had diversified, demonstrating a deep genetic history of dogs during the Paleolithic. Coanalysis with human genomes reveals aspects of dog population history that mirror humans, including Levant-related ancestry in Africa and early agricultural Europe. Other aspects differ, including the impacts of steppe pastoralist expansions in West and East Eurasia and a near-complete turnover of Neolithic European dog ancestry. [1]: /lookup/doi/10.1126/science.aba9572 [2]: /lookup/doi/10.1126/science.abe7823


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Fernando Alonso has told Sky Sports Williams driver George Russell is his pick for the future among the sport's emerging young crop of drivers.


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Lewis Hamilton has spoken passionately of his desire to have more difficult races like the Turkish GP so he can prove


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14.4k

Sergio Perez will not be able to race in this weekend's British Grand Prix at Silverstone after he tested positive for Covid-19.


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11.9k

Fernando Alonso is set to make his F1 comeback with Renault in 2021. And the two-time world champion believes that the team – who will be rechristened as Alpine next season – will getting one of the sport’s most complete drivers when he joins them for next year.


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8.59k

Six-time world champion Lewis Hamilton has used his social media platforms to speak out on racism and diversity, and called for Formula 1 to do more. F1 motorsports boss Ross Brawn says he fully backs the Mercedes driver’s comments…


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The Vietnam GP will not feature on the 2021 Formula 1 calendar.


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Sky F1's Jenson Button believes Lewis Hamilton would relish greater competition in the future, as his former team-mate bids to build on an


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7.11k

Lewis Hamilton is giving serious consideration to calling time on his long and glittering Formula One career at the end of the current season


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7.08k

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Early in the pandemic, the Louisiana Department of Health started sending out lists of patients who tested positive for the coronavirus to local emergency officials, in an effort to help


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Sergio Perez has admitted that securing a Red Bull drive alongside Max Verstappen is now his only option to remain in Formula 1 for 2021, and says he would relish the chance of nailing down the


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With the victories still coming thick and fast despite being in his 14th season, Hamilton has admitted that he’s enjoying being an F1 driver as much as ever – and not relishing the prospect of hanging up his helmet when the time comes...


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Lewis Hamilton will have his first chance to equal Michael Schumacher's illustrious record of seven F1 world titles at the Turkish Grand Prix this Sunday.


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George Russell said praise from Fernando Alonso meant


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Lewis Hamilton believes his battles with Max Verstappen will only intensify over the next 12 months with F1's champion expecting Mercedes and Red Bull to remain as close as recent races.


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5.88k

Lewis Hamilton has opened up on his Formula 1 future in an exclusive interview with Sky Sports, admitting he is unsure how much longer he will remain in the sport but that he


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5.83k

Formula 1 welcomes back another


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5.06k

The current global pandemic of coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A critical initial step of infection is the interaction of the virus with receptors on host cells. In the case of SARS-CoV-2 and other coronaviruses, this receptor binding occurs through the spike (S) protein on the virus surface. Both SARS-CoV-2 and the related SARS-CoV, which caused an outbreak in 2003, bind to angiotensin-converting enzyme 2 (ACE2) on human cells. However, the observed differences in tissues that are infected by these two viruses (tropism) suggests that additional host factors may be involved. On pages 861 and 856 of this issue, Daly et al. ([ 1 ][1]) and Cantuti-Castelvetri et al. ([ 2 ][2]), respectively, show that the membrane protein neuropilin-1 (NRP1) promotes SARS-CoV-2 entry and explain how NRP1 interacts with the SARS-CoV-2 S protein. The results suggest the S protein–NRP1 interaction as a potential antiviral target. Coronaviruses are enveloped RNA viruses that can cause human diseases that range from the common cold to severe and fatal respiratory infections. It is thought that both SARS-CoV-2 and SARS-CoV bind to ACE2 on the host cell surface, are internalized by endocytosis, and fuse with the endolysosome membrane to deliver the viral genome for replication in the host cell ([ 3 ][3], [ 4 ][4]) (see the figure). The viral S protein mediates this key membrane fusion reaction, but its activity requires several processing steps. S is synthesized as a large membrane protein that is cleaved into two components, S1 and S2, which remain noncovalently associated ([ 5 ][5], [ 6 ][6]). Cleavage is required for infection and can occur during virus particle production or virus entry into the target cell. The S1 protein forms the “head” of the molecule and mediates binding to ACE2. The S2 protein is anchored in the virus membrane and mediates membrane fusion. S2, like the fusion proteins of influenza virus and HIV-1, inserts a hydrophobic fusion peptide at its amino terminus into the cell membrane and then folds back to merge the host and virus membranes ([ 7 ][7]). The S2 protein needs a further proteolytic step to “liberate” its fusion peptide, and this is carried out by transmembrane protease serine 2 (TMPRSS2) or other proteases ([ 3 ][3]). A potentially important difference between SARS-CoV-2 and SARS-CoV is the mechanism of S protein cleavage into S1 and S2. In SARS-CoV, this is caused by host cell proteases called cathepsins, which are located within endocytic compartments. However, the sequence of the SARS-CoV-2 S protein contains a series of basic amino acids at the S1-S2 junction. Such polybasic sites can be substrates for furin, a protease that is present in the secretory pathway and endocytic compartments ([ 8 ][8]). Studies with SARS-CoV-2 show that its S protein is cleaved by furin during virus production and that this cleavage promotes subsequent virus infection ([ 3 ][3], [ 6 ][6]). Thus, a notable difference between the S proteins of these two coronaviruses is the protease that carries out the S1-S2 cleavage reaction. Furin cleavage also produces a potentially important remnant: the polybasic site that remains at the carboxyl terminus of SARS-CoV-2 S1 after cleavage. Neuropilins are a family of membrane proteins that were originally identified because of their involvement in angiogenesis (blood vessel formation) and axon guidance ([ 9 ][9]). The neuropilins are co-receptors for molecules such as vascular endothelial growth factors (VEGFs) and semaphorins, and recent studies have demonstrated their up-regulation during tumor angiogenesis and their potential as anticancer targets. Both NRP1 and NRP2 can bind the carboxyl-terminal sequences generated by furin processing of molecules such as VEGFs, with the sequences fitting into a pocket on the b1 domain of the NRP ([ 9 ][9]). Detailed studies of such NRP1-peptide interactions show that binding to the b1 pocket requires the sequence Arg/Lys-X-X-Arg/Lys (R/K-XX-R/K, where X can be any amino acid) at the carboxyl terminus of the protein or peptide ([ 10 ][10]). This “C-end rule,” or CendR, can thus predict whether a protein is a candidate for binding to NRPs. Daly et al. and Cantuti-Castelvetri et al. found that the sequence of the S1-S2 junction of virus isolates from human patients suggested that they fit the C-end rule, with Arg-Arg-Ala-Arg (RRAR) predicted to form the carboxyl-terminal sequence of the furin-cleaved S1. They showed that NRP1 promoted infection of human cell lines by SARS-CoV-2 and by lentivirus pseudotypes that contained the SARS-CoV-2 S protein on their surface. NRP1 was not the only host factor that promoted SARS-CoV-2 infection, but even when both ACE2 and TMPRSS2 were present, NRP1 gave an additional increase. This was due to an increase in virus uptake into the cell rather than an increase in virus binding to the cell surface. The promotion of virus infection by NRP1 was inhibited by the addition of a soluble NRP1 or by an antibody that mapped to the binding pocket on NRP1. Further analyses revealed that S1 or its carboxyl-terminal region interact with NRP1, and this was inhibited by mutations in the NRP b1 pocket. SARS-CoV-2 mutants in which the polybasic cleavage site was deleted or S was made resistant to furin cleavage were insensitive to NRP1 expression. ![Figure][11] Model for SARS-CoV-2 processing and entry Proteolytic processing of SARS-CoV and SARS-CoV-2 S proteins facilitates virus entry. SARS-CoV and SARS-CoV-2 bind to ACE2 at a region on S1. Furin cleavage at the S1-S2 junction exposes the C-end rule peptide on SARS-CoV-2 S1 and allows binding to NRP1. Subsequent processing by cathepsins and TMPRSS2 allows S2 fusion peptide–mediated membrane insertion and merging of membranes. The absence of a furin cleavage site in SARS-CoV S1 and a SARS-CoV-2 S1 mutant prevents binding to NRP1 and limits virus entry and infection. GRAPHIC: V. ALTOUNIAN/ SCIENCE Daly et al. showed that a peptide derived from the S1 carboxyl terminus binds to the NRP1 b1 domain with micromolar affinity. They solved the crystal structure of the complex, which revealed that the peptide is positioned in the b1 pocket, similar to a VEGF peptide that was crystallized with b1 ([ 9 ][9]). A small-molecule antagonist of NRP1 that inhibits VEGF binding ([ 11 ][12]) also inhibited the b1-S1 peptide interaction and virus infection. C-end rule peptides had previously been shown to mediate uptake of particles or bacteriophages by cells and tissues ([ 10 ][10]). Cantuti-Castelvetri et al. conjugated the S1 peptide onto nanoparticles and administered them intranasally to mice. The mouse olfactory epithelium expresses NRP1, and the authors observed significant uptake of the peptide-conjugated particles in this site. Similar to previous results ([ 10 ][10]), the S1 peptide–coated particles were observed to also travel into the neurons and blood vessels of the cortex. To address the possible role of NRP1 in human SARS-CoV-2 infection, the authors used available data to confirm expression of both NRP1 and NRP2 RNA in human lung and olfactory epithelial tissue. They also showed that five out of six autopsy samples of olfactory epithelia from human COVID-19 patients were positive for both S protein and NRP1. These results from mice and humans are intriguing given that many COVID-19 patients lose their sense of smell. Together, these papers establish NRP1 as a host factor for SARS-CoV-2 and suggest interesting parallels and differences with the roles of NRPs in infection by other viruses. For example, both the human T cell lymphotropic virus SU protein and the Epstein Barr virus (EBV) gB protein are processed by furin, and infection by these viruses is promoted by NRP1 ([ 12 ][13], [ 13 ][14]). EBV, which infects nasopharyngeal epithelial cells, shows an apparent reciprocal effect in which NRP1 promotes infection, whereas NRP2 inhibits it ([ 13 ][14]). Although Daly et al. showed that S1 protein can also bind NRP2, its role in SARS-CoV-2 infection is unknown. NRP2 is a receptor for Lujo virus, but this does not involve binding to the b1 pocket ([ 14 ][15]). These and other examples indicate that a number of viruses have evolved to use NRPs during infection, but much remains unclear. There is more to learn about the promotion of SARS-CoV-2 infection by NRP1. The virus can propagate in the absence of furin cleavage in some cultured cells, where cathepsin cleavage may be sufficient, but in vivo, the virus relies on furin processing, which enhances viral pathogenesis in a hamster model ([ 15 ][16]). How does NRP1 binding affect the virus internalization pathway, and does it act as a co-receptor with ACE2? C-end rule peptide binding to NRP1 can promote vascular leakage and tissue penetration, especially when the peptides are presented on a multivalent particle ([ 10 ][10]). Does NRP1 similarly help to promote SARS-CoV-2 dissemination and spread? Together, Daly et al. and Cantuti-Castelvetri et al. show that furin processing, which has an important role in the maturation and fusion activity of the SARS-CoV-2 S protein, also acts to generate ligands on the virus particle that bind NRP1. The availability of small molecule inhibitors of the NRP1-C-end rule peptide interaction suggests a potential antiviral strategy. Defining the importance of this interaction in vivo will be a vital next step. 1. [↵][17]1. J. L. Daly et al ., Science 370, 861 (2020). [OpenUrl][18][Abstract/FREE Full Text][19] 2. [↵][20]1. L. Cantuti-Castelvetri et al ., Science 370, 856 (2020). [OpenUrl][21][Abstract/FREE Full Text][22] 3. [↵][23]1. M. Hoffmann et al ., Cell 181, 271 (2020). [OpenUrl][24][CrossRef][25][PubMed][26] 4. [↵][27]1. X. Ou et al ., Nat. Commun. 11, 1620 (2020). [OpenUrl][28][CrossRef][29][PubMed][26] 5. [↵][30]1. D. Wrapp et al ., Science 367, 1260 (2020). [OpenUrl][31][Abstract/FREE Full Text][32] 6. [↵][33]1. A. C. Walls et al ., Cell 181, 281 (2020). [OpenUrl][34][CrossRef][35][PubMed][26] 7. [↵][36]1. S. C. Harrison , Virology 479–480C, 498 (2015). [OpenUrl][37][CrossRef][38][PubMed][39] 8. [↵][40]1. S. S. Molloy et al ., Trends Cell Biol. 9, 28 (1999). [OpenUrl][41][CrossRef][42][PubMed][43][Web of Science][44] 9. [↵][45]1. H. F. Guo, 2. C. W. Vander Kooi , J. Biol. Chem. 290, 29120 (2015). [OpenUrl][46][Abstract/FREE Full Text][47] 10. [↵][48]1. T. Teesalu et al ., Proc. Natl. Acad. Sci. U.S.A. 106, 16157 (2009). [OpenUrl][49][Abstract/FREE Full Text][50] 11. [↵][51]1. A. Jarvis et al ., J. Med. Chem. 53, 2215 (2010). [OpenUrl][52][CrossRef][53][PubMed][54] 12. [↵][55]1. S. Lambert et al ., Blood 113, 5176 (2009). [OpenUrl][56][Abstract/FREE Full Text][57] 13. [↵][58]1. H. B. Wang et al ., Nat. Commun. 6, 6240 (2015). [OpenUrl][59][CrossRef][60][PubMed][61] 14. [↵][62]1. M. Raaben et al ., Cell Host Microbe 22, 688 (2017). [OpenUrl][63][CrossRef][64][PubMed][65] 15. [↵][66]1. S. Y. Lau et al ., Emerg. Microbes Infect. 9, 837 (2020). [OpenUrl][67][CrossRef][68][PubMed][69] Acknowledgments: The author is supported by National Institutes of Health (R01-GM057454 and R01-AI075647). 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{openurl}?query=rft.jtitle%253DNat.%2BCommun.%26rft.volume%253D11%26rft.spage%253D1620%26rft_id%253Dinfo%253Adoi%252F10.1038%252Fs41467-020-15562-9%26rft_id%253Dinfo%253Apmid%252Fhttp%253A%252F%252Fwww.n%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [29]: /lookup/external-ref?access_num=10.1038/s41467-020-15562-9&link_type=DOI [30]: #xref-ref-5-1 "View reference 5 in text" [31]: {openurl}?query=rft.jtitle%253DScience%26rft_id%253Dinfo%253Adoi%252F10.1126%252Fscience.abb2507%26rft_id%253Dinfo%253Apmid%252F32075877%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [32]: 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{openurl}?query=rft.jtitle%253DVirology%26rft.volume%253D479480%26rft.spage%253D498%26rft_id%253Dinfo%253Adoi%252F10.1016%252Fj.virol.2015.03.043%26rft_id%253Dinfo%253Apmid%252F25866377%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [38]: /lookup/external-ref?access_num=10.1016/j.virol.2015.03.043&link_type=DOI [39]: /lookup/external-ref?access_num=25866377&link_type=MED&atom=%2Fsci%2F370%2F6518%2F765.atom [40]: #xref-ref-8-1 "View reference 8 in text" [41]: 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Reinfection, in which an individual is subject to multiple, distinct infections from the same virus species throughout their lifetime, is a salient feature of many respiratory viruses. Indeed, the persistence and ubiquity in human society of common respiratory viruses—including influenza viruses, respiratory syncytial virus (RSV), rhinovirus, and the endemic coronaviruses—are largely due to their ability to produce repeat infection. Since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for the ongoing coronavirus disease 2019 (COVID-19) pandemic, a critical concern has been whether humans will experience reinfections with this pathogen, which might enable it to become endemic. Typically, following an initial infection, the human adaptive immune system develops a suite of defenses, including memory B lymphocytes capable of producing neutralizing antibodies targeted to bind to that particular pathogen, and memory T lymphocytes that help regulate immune responses and induce death of infected cells. These adaptive immune components, particularly B cells, can produce sterilizing immunity in which the pathogen, if reintroduced to the host, is prevented from replicating within the body. However, for many viruses, a number of processes, particularly insufficient adaptive immune response, waning immunity, and immune escape, can undermine or circumvent the sterilizing character of immunity and allow subsequent reinfection. In the first instance, an initial infection with a particular agent may not engender an adaptive immune response sufficient to confer sterilizing immunity. Serological studies indicate that most SARS-CoV-2 infections, regardless of severity, induce development of some specific antibodies ([ 1 ][1]); however, despite encouraging results from the experimental vaccination of primates, it remains unclear whether those antibodies are sufficient to provide long-term effective protection or if other adaptive immune components are present and functional. Furthermore, immune response to SARS-CoV-2 infection is heterogeneous, with individuals who experience asymptomatic infections manifesting a weaker immune response than those experiencing more severe disease ([ 1 ][1]). It is possible that some individuals never develop sterilizing immunity following infection with SARS-CoV-2, or that multiple exposures will be needed for affinity maturation and development of long-lasting protection. ![Figure][2] Factors influencing postpandemic transmission of SARS-CoV-2 Rates of repeat infection, factors modulating seasonality, competition with other circulating respiratory viruses, and control measures will influence the endemic pattern of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission. GRAPHIC: C. BICKEL/ SCIENCE Waning immunity, in which the initial adaptive immune response is robust and protective but dissipates over time, leaving the host vulnerable to reinfection, may also undermine sterilizing immunity. Immune escape is a third process that can facilitate reinfection, in particular by viruses. Here, a virus, during its continued serial passage through a host population, accumulates point mutations. This accumulation, termed antigenic drift, may lead to conformational changes of viral surface proteins that disrupt the binding of antibodies previously generated against an earlier variant. Immune escape is a consequence of this antigenic drift that enables reinfection through the evasion of adaptive protection. The time scales of waning immunity and immune escape differ by pathogen and have yet to be defined for SARS-CoV-2. Thus far, the mutation rate of the SARS-CoV-2 genome appears to be slower than that of influenza viruses. This lower rate may be a consequence of proof-reading during replication, which is exclusive to coronaviruses among RNA viruses. Conversely, human coronavirus (HCoV) OC43 is highly variable, particularly in genes encoding surface proteins such as the spike protein, indicating that considerable diversification can occur. To date, some evidence of SARS-CoV-2-specific antibody waning has been captured in a longitudinal study ([ 2 ][3]), and a few verified repeat SARS-CoV-2 infections have been documented ([ 3 ][4]). Although reinfections can occur, the number of reinfection cases is not currently sufficient to generalize the duration of immunity at population scales or the severity of repeat infection. Whether reinfections will be commonplace, how often they will occur, how contagious reinfected individuals will be, and whether the risk of severe clinical outcomes changes with subsequent infection remain to be understood. Insight from other respiratory viruses points to the possibility of reinfection with SARS-CoV-2. Naturally acquired infections with the four endemic HCoVs (OC43, HKU1, 229E, and NL63) indicate that reinfections with the same HCoV type are common within 1 year ([ 4 ][5]); sequential infections with the same influenza virus strain can occur in less than 2 years ([ 5 ][6]); and reinfections of adults with RSV within 1 year have also been documented ([ 6 ][7]). By contrast, more pathogenic viruses that induce systemic effects on the host may elicit a longer-lasting adaptive immune response. For example, longitudinal immune profiles from SARS survivors showed a stronger immune response with neutralizing antibodies persisting for 2 to 5 years ([ 7 ][8]). However, it could not be confirmed if and for how long this response conferred immunity because the SARS outbreak lasted less than 1 year. In addition to duration of protective immunity, the long-term effects of SARS-CoV-2 on humans will depend on the severity of reinfection. Sequential infections with influenza virus have been associated with less severe symptoms ([ 8 ][9]), whereas no association between reinfection and symptom severity was found in recurring endemic HCoV infections ([ 4 ][5]). In addition, for other viruses (e.g., RSV and dengue), suboptimal binding of naturally induced or vaccine-induced antibodies can enhance infection severity upon subsequent exposure, a phenomenon called antibody-dependent enhancement (ADE) ([ 9 ][10]). To date, responses among the few patients with verified SARS-CoV-2 reinfection have been heterogeneous with one apparent repeat infection requiring hospitalization. Thus, thorough serological and prospective studies are needed to determine whether ADE manifests among SARS-CoV-2 infections, either because of prior homologous infection or cross-reactive antibodies from other HCoVs. This will have particular relevance for vaccines and convalescent plasma therapy. Should reinfection prove commonplace, and barring a highly effective vaccine delivered to most of the world's population, SARS-CoV-2 will likely become endemic ([ 10 ][11]). The typical time scale at which individuals experience reinfection and seasonal differences in transmissibility will determine the pattern of endemicity. Outside the tropics, the incidence of many common respiratory virus infections increases during particular times of the year. This phase-locked behavior is due to accumulated susceptibility to reinfection, which increases over time because of immune escape and waning immunity, and seasonal modulation of virus transmissibility derived from environmental conditions, changing behavior (e.g., mixing indoors in cold weather), or altered immune function. For example, influenza incidence is greatest during winter in temperate regions. Once expelled from an infectious host, the influenza virus appears to be more stable in low-humidity conditions ([ 11 ][12]), which are prevalent both indoors and outdoors during winter. Further, during colder months, people spend more time indoors and school is in session, which may facilitate transmission, and shorter days and less sunlight exposure may suppress immune function. The endemic HCoVs (OC43, HKU1, NL63, and 229E) all exhibit a seasonality in temperate regions, similar to influenza viruses ([ 12 ][13]). Consequently, numerous studies have sought to determine whether conditions such as temperature, sunlight, humidity, ozone, and pollution affect SARS-CoV-2 viability and transmissibility. The results are not currently conclusive, although it appears that environmental conditions, such as sunlight and humidity, may modulate SARS-CoV-2 transmissibility—not enough to preclude transmission during the first waves of the pandemic when immunity is generally low—but perhaps sufficient to favor seasonal, phase-locked transmission during winter in temperate regions, similar to influenza virus, once immunity increases. Like the 2009 influenza pandemic, the continued circulation by SARS-CoV-2 following this initial pandemic period will manifest as a function of reinfection rates, vaccine availability and efficacy, and social, immune, and innate factors that modulate virus transmissibility (see the figure). In addition, the cyclic persistence of SARS-CoV-2 in human populations may be affected by ongoing opportunities for interaction with other respiratory pathogens. Co-circulating respiratory viruses may interfere with one another while competing for the same resources, and their interactions have been studied at population and individual levels, in reconstructed human tissues and in animal models. The outcomes in individuals experiencing serial exposure to different viruses vary and in general appear to depend on the order and timing of exposures. Many studies have documented evidence of negative interference between viruses caused by short-lived (days) protection elicited from the first infection. Host antiviral interferon responses are often regarded as the main mechanism by which interference manifests; that is, as a result of a recent infection, the host cells up-regulate the synthesis of interferons, potentially inhibiting a secondary infection. Even though it is short-lived, this effect can be strong at population scales and temporarily reduce the prevalence of a virus or shift the timing of its circulation. For example, it is hypothesized that a large summer 2009 rhinovirus outbreak delayed pandemic influenza virus emergence in Europe ([ 13 ][14]). The clinical and population-scale interactions of SARS-CoV-2 with other respiratory viruses, particularly influenza viruses and other HCoVs, need to be monitored in the coming years. To date, some SARS-CoV-2 coinfections have been documented ([ 14 ][15]), including coinfections with influenza and RSV; however, testing for multiple pathogens has not been routinely carried out, and the scarce data that do exist, mostly for older adults with high rates of preexisting medical conditions, do not support a definitive evaluation of coinfection likelihood or severity. Studies prior to the pandemic indicate that simultaneous infections with multiple respiratory viruses are not uncommon but are not associated with increased disease severity. At the population scale, a possible overlap between influenza and SARS-CoV-2 outbreaks poses a serious threat to public health systems. Seasonal influenza produces millions of severe infections worldwide every year, and this additional burden could be catastrophic on systems already challenged by the COVID-19 pandemic. Conversely, given similar modes of transmission among different respiratory viruses, the nonpharmaceutical interventions adopted to mitigate SARS-CoV-2 transmission (personal protective equipment, social distancing, increased hygiene, limited indoor gatherings) may reduce the magnitude of seasonal influenza outbreaks. Such increased use of nonpharmaceutical measures, and possible virus interference, could be responsible for the reduced incidence of influenza during the recent winter of the Southern Hemisphere ([ 15 ][16]). The phases and magnitudes of different outbreaks in a multipathogen system are dictated by the interaction dynamics between those pathogens: from large overlapping phases when pathogens enhance one another's transmission, to complete inhibition of a strain by the neutralizing cross-reactivity of a more transmissible one ([ 9 ][10]). Several postpandemic scenarios for SARS-CoV-2 have been modeled ([ 10 ][11]), postulated on duration of immunity and cross-immunity between SARS-CoV-2 and the other betacoronaviruses (OC43 and HKU1). A duration of immunity similar to that of the other betacoronaviruses (∼40 weeks) could lead to yearly outbreaks of SARS-CoV-2, whereas a longer immunity profile, coupled with a small degree of protective cross-immunity from other betacoronaviruses, could lead to the apparent elimination of the virus followed by resurgence after a few years. Other scenarios are, of course, possible, because there are many processes at play and much that remains unresolved. 1. 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[OpenUrl][42][Abstract/FREE Full Text][43] 10. [↵][44]1. S. M. Kissler, 2. C. Tedijanto, 3. E. Goldstein, 4. Y. H. Grad, 5. M. Lipsitch , Science 368, 860 (2020). [OpenUrl][45][Abstract/FREE Full Text][46] 11. [↵][47]1. J. Shaman, 2. M. Kohn , Proc. Natl. Acad. Sci. U.S.A. 106, 3243 (2009). [OpenUrl][48][Abstract/FREE Full Text][49] 12. [↵][50]1. A. S. Monto et al ., J. Infect. Dis. 222, 9 (2020). [OpenUrl][51][CrossRef][52][PubMed][53] 13. [↵][54]1. A. Wu et al ., Lancet Microbe 10.1016/S2666-5247(20)30114-2 (2020). 14. [↵][55]1. D. Kim, 2. J. Quinn, 3. B. Pinsky, 4. N. H. Shah, 5. I. Brown , JAMA 323, 2085 (2020). [OpenUrl][56][CrossRef][57][PubMed][58] 15. [↵][59]WHO, [www.who.int/influenza/surveillance\_monitoring/updates/2020\_08\_31\_update\_GIP\_surveillance/en/][60] (2020). Acknowledgments: J.S. and Columbia University partially own SK Analytics. J.S. consults for BNI. This work was supported by U.S. National Science Foundation grant DMS-2027369 and a gift from the Morris-Singer Foundation. 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Much effort is being targeted at developing vaccines that will provide protection against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A trimeric spike protein that decorates the virus is a primary target of the host immune system and the focus of vaccine development. Bangaru et al. present the structure of a leading vaccine candidate: a full-length spike protein with some modifications aimed at enhancing stability that is formulated in polysorbate 80 detergent. The study confirms that the full-length immunogen is in a stable prefusion conformation and provides a basis for understanding immune responses to the vaccine. Science , this issue p. [1089][1] Vaccine efforts to combat the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is responsible for the current coronavirus disease 2019 (COVID-19) pandemic, are focused on SARS-CoV-2 spike glycoprotein, the primary target for neutralizing antibodies. We performed cryo–election microscopy and site-specific glycan analysis of one of the leading subunit vaccine candidates from Novavax, which is based on a full-length spike protein formulated in polysorbate 80 detergent. Our studies reveal a stable prefusion conformation of the spike immunogen with slight differences in the S1 subunit compared with published spike ectodomain structures. We also observed interactions between the spike trimers, allowing formation of higher-order spike complexes. This study confirms the structural integrity of the full-length spike protein immunogen and provides a basis for interpreting immune responses to this multivalent nanoparticle immunogen. [1]: /lookup/doi/10.1126/science.abe1502


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Political polarization, a concern in many countries, is especially acrimonious in the United States (see the first box). For decades, scholars have studied polarization as an ideological matter—how strongly Democrats and Republicans diverge vis-à-vis political ideals and policy goals. Such competition among groups in the marketplace of ideas is a hallmark of a healthy democracy. But more recently, researchers have identified a second type of polarization, one focusing less on triumphs of ideas than on dominating the abhorrent supporters of the opposing party ([ 1 ][1]). This literature has produced a proliferation of insights and constructs but few interdisciplinary efforts to integrate them. We offer such an integration, pinpointing the superordinate construct of political sectarianism and identifying its three core ingredients: othering, aversion, and moralization. We then consider the causes of political sectarianism and its consequences for U.S. society—especially the threat it poses to democracy. Finally, we propose interventions for minimizing its most corrosive aspects. Democrats and Republicans—t he 85% of U.S. citizens who do not identify as pure independents—have grown more contemptuous of opposing partisans for decades, and at similar rates [see supplementary materials (SM)]. Only recently, however, has this aversion exceeded their affection for copartisans. On a “feeling thermometer” scale ranging from cold (0°) to neutral (50°) to warm (100°), affect toward copartisans has consistently hovered in the 70° to 75° range. By contrast, affect toward opposing partisans has plummeted from 48° in the 1970s to 20° today (see the figure, top panel). And cold feelings toward the out-party now exceed warm feelings toward the in-party (see the figure, bottom panel). Out-part y hate has also become more powerful than in-party love as a predictor of voting behavior ([ 2 ][2]), and by some metrics, it exceeds long-standing antipathies around race and religion (SM). This aversion to opposing partisans might make strategic sense if partisan identity served as a strong proxy for political ideas. But given that sectarianism is not driven primarily by such ideas (SM), holding opposing partisans in contempt on the basis of their identity alone precludes innovative cross-party solutions and mutually beneficial compromises. This preclusion is unfortunate, as common ground remains plentiful. Indeed, despite the clear evidence that partisans have grown increasingly disdainful of one another, the evidence that they have polarized in terms of policy preferences is equivocal ([ 3 ][3]). Along the way, the causal connection between policy preferences and party loyalty has become warped, with partisans adjusting their policy preferences to align with their party identity (SM). For example, a recent experiment demonstrated that Republicans exhibit a liberal attitude shift after exposure to a clip of President Donald Trump voicing a liberal policy position (SM); there is little evidence to suggest that Democrats are immune to analogous shifts in response to their own political leaders. Overall, the severity of political conflict has grown increasingly divorced from the magnitude of policy disagreement ([ 4 ][4]). #### On American exceptionalism A recent study offers valuable international perspective on political polarization, leveraging data from 1975 through 2017 in nine Western democracies to examine feelings toward copartisans and opposing partisans. The study controls statistically for the number of parties and offers a valuable, albeit noncomprehensive, comparison set ([ 13 ][5]). Four nations—America, Canada, New Zealand, and Switzerland—exhibit increasing sectarianism over time, with the rate steepest in America. By contrast, Australia, Britain, Norway, Sweden, and Germany exhibit decreasing sectarianism over time. The most notable findings pertain to out-party hate [increasingly “frigid” evaluations of opposing partisans, via a “feeling thermometer” (see main text)]. Across the eight other nations, the mean rate of change in out-party hate was 0.004° per year (range: −0.2° to +0.2°) on the 0°-to-100° scale. In the United States, the rate of change was −0.6° per year. By 2017, out-party hate was stronger in America than in any other nation. In the past decade, political scientists have introduced various constructs to capture this nonideological type of polarization, including “affective polarization” ([ 1 ][1]) and “social polarization” ([ 4 ][4]). Scholars from psychology and other disciplines have introduced constructs, such as “tribalism” (SM), to flesh out its social-psychological properties. We propose here a superordinate construct, political sectarianism—the tendency to adopt a moralized identification with one political group and against another. Whereas the foundational metaphor for tribalism is kinship, the foundational metaphor for political sectarianism is religion, which evokes analogies focusing less on genetic relatedness than on strong faith in the moral correctness and superiority of one's sect. Political identity is secondary to religion in traditional forms of sectarianism, but it is primary in political sectarianism. In the United States today, even though Democrats and Republicans differ on average in terms of religious affiliation, their schism is fundamentally political rather than religious. It is, in this sense, quite distinct from the Sunniversus-Shia sectarian schisms that characterize politics in some Muslim-majority nations. Political sectarianism consists of three core ingredients: othering—the ten dency to view opposing partisans as essentially different or alien to oneself; aversion—the tendency to dislike and distrust opposing partisans; and moralization—the tendency to view opposing partisans as iniquitous. It is the confluence of these ingredients that makes sectarianism so corrosive in the political sphere. Viewing opposing partisans as different, or even as dislikable or immoral, may not be problematic in isolation. But when all three converge, political losses can feel like existential threats that must be averted—whatever the cost. Rising political sectarianism in the United States is multiply determined; here we consider three crucial causes. First, in recent decades, the nation's major political parties have sorted in terms of ideological identity and demography. Whereas self-identified liberals and conservatives used to be distributed broadly between the two parties, today the former are overwhelmingly Democrats and the latter are overwhelmingly Republicans (SM) . The parties also have sorted along racial, religious, educational, and geographic lines. Although far from absolute, such alignment of ideological identities and demography transforms political orientation into a mega-identity that renders opposing partisans different from, even incomprehensible to, one another ([ 4 ][4]). This mega-identity can grow so powerful that it changes other identities, as when partisans alter their self-identified religion, class, or sexual orientation to align with their political identity (SM). ![Figure][6] The rise of out-party hate With the exception of 2020, all data come from the American National Election Study (ANES), as reported in ([ 1 ][1]). To calculate the estimates for the lower panel, we used upper-panel estimates to compute, relative to the neutral point on the feeling thermometer, the strength of in-party love (in-party score − 50) and out-party hate (50 − out-party score), and then took the difference of those two scores. See supplementary materials for details. GRAPHIC: N. CARY/ SCIENCE As distinct as Democrats and Republicans actually are today, partisans nevertheless vastly overestimate such differences. They view opposing partisans as more socially distant, ideologically extreme, politically engaged, contemptuous, and uncooperative than is actually the case ([ 5 ][7]) (SM), thereby exacerbating political sectarianism. For example, Republicans estimate that 32% of Democrats are LGBT when in reality it is 6%; Democrats estimate that 38% of Republicans earn over $250,000 per year when in reality it is 2% ([ 6 ][8]). Second, as Americans have grown more receptive to consuming information slanted through a partisan lens, the media ecosystem has inflamed political sectarianism. The decline of the broadcast news era, during which impartiality was prized, began in the 1980s, driven in part by the Reagan administration's termination of the Federal Communications Commission (FCC) “fairness doctrine” in 1987. This doctrine, introduced in 1949, required that broadcasters discuss controversial topics in a manner that the FCC assesses as unbiased. Among the first media figures to leverage the demise of the fairness doctrine was Rush Limbaugh, whose influential conservative radio program went into national syndication in 1988 (SM). The ethos of impartiality that CNN espoused when introducing cable news faltered with the launch of the conservative Fox News in 1996 and the liberal pivot of MSNBC a decade later. People w ho are already sectarian selectively seek out congenial news, but consuming such content also amplifies their sectarianism (SM). In recent years, social media companies like Facebook and Twitter have played an influential role in political discourse, intensifying political sectarianism. Scholars from sociology, political science, economics, psychology, and computational social science debate whether such web platforms create polarizing echo chambers ([ 7 ][9]) (SM). However, a recent field experiment offers intriguing evidence that Americans who deactivate their Facebook account become less politically polarized ([ 8 ][10]). In addition, emotional and moralized posts—those containing words like “hate,” “shame,” or “greed”—are especially likely to be retweeted within rather than between partisan networks ([ 9 ][11]). Social-media technology employs popularity-based algorithms that tailor content to maximize user engagement, increasing sectarianism within homogeneous networks (SM), in part because of the contagious power of content that elicits sectarian fear or indignation. Third, i n contrast to the equivocal ideological-polarization trends among the public, politicians and other political elites have unambiguously polarized recently on ideological grounds, with Republican politicians moving further to the right than Democratic politicians have moved to the left (SM). This ideological divergence is driven in part by extreme economic inequality in America today, especially in conjunction with candidates becoming increasingly reliant on ideologically extreme donors. As politicians chase campaign dollars, these extreme voices garner disproportionate influence (SM). The ideological divergence of political elites contributes to political sectarianism, especially as these individuals increasingly use disciplined messaging to discuss their preferred topics in their preferred manner (SM). Such messaging leads the public to perceive sharper ideological distinctions between the parties than actually exists, which inflames sectarianism (SM). In addition, Newt Gingrich and his followers achieved electoral success with strongly moralized language in the 1980s and 1990s, inspiring political elites on both sides to double down on the rhetoric of moral outrage (e.g., “disgraceful,” “shameful”), further exacerbating sectarianism (SM). These three trends—identity alignment, the rise of partisan media, and elite ideological polarization—have contributed to radically different sectarian narratives about American society and politics. Although the content of these narratives is entirely different across the political divide, their structure is similar: The other side cheats, so our side would be foolish to adhere to long-standing democratic norms. These narratives, which partisans experience less as stories than as truth (SM), increase their willingness to sacrifice those norms in pursuit of partisan ends. Rising political sectarianism has, not surprisingly, increased the social distance between Democrats and Republicans. Compared to a few decades ago, Americans today are much more opposed to dating or marrying an opposing partisan; they are also wary of living near or working for one. They tend to discriminate, as when paying an opposing partisan less than a copartisan for identical job performance or recommending that an opposing partisan be denied a scholarship despite being the more qualified applicant ([ 1 ][1]). They are also susceptible to motivated partisan cognition—seeking out, believing, and approving of information more readily when it reflects positively on copartisans or negatively on opposing partisans ([ 10 ][12]) (SM)—although scholars debate whether such tendencies are equally strong among Democrats and Republicans (see the second box). These manifestations of political sectarianism echo those that emerge from religious sectarianism. What is distinctive about political sectarianism—beyond its largely nontheological foundation—is the immediacy of its links to governance. Political sectarianism compromises the core government function of representation. Because sectarian partisans almost never vote for the opposition, politicians lack the incentive to represent all of their constituents. Straight-ticket voting has grown increasingly widespread. In contested districts, the correlation of the Democratic share of the House vote and the Democratic share of the presidential vote—the association of district-level with national representation—surged from 0.54 in the 1970s to 0.94 by the 2010s ([ 2 ][2]). Perhaps most troubling of all, the political sectarianism of the public incentivizes politicians to adopt antidemocratic tactics when pursuing electoral or political victories. A recent experiment shows that, today, a majority-party candidate in most U.S. House districts—Democrat or Republican—could get elected despite openly violating democratic principles like electoral fairness, checks and balances, or civil liberties ([ 11 ][13]). Voters' decisions to support such a candidate may seem sensible if they believe the harm to democracy from any such decision is small while the consequences of having the vile opposition win the election are catastrophic. However, the accumulation of such choices undermines representative democracy. And a society that pretends to adhere to democratic principles but actually does not is one in which people who possess resources and influence can leverage democratic gray zones to impose their will on those who do not. Sectarianism stimulates activism (SM), but also a willingness to inflict collateral damage in pursuit of political goals (SM) and to view copartisans who compromise as apostates (SM). As political sectarianism has surged in recent years, so too has support for violent tactics (SM). In addition , highly sectarian partisans are vulnerable to exploitation. In 2016, Russia sought to stoke partisan outrage during America's election by creating fake social-media avatars with names like “Blacktivist” and “army\_of\_jesus.” These efforts succeeded in duping sectarian extremists—especially those who were older and more conservative than average—into amplifying the avatars' memes about the depravity of opposing partisans (SM). In doing so, these partisans served as pawns in Russia's efforts to weaken America. #### Is motivated partisan cognition bipartisan? The extent to which each side exhibits motivated partisan (or biased) cognition is a focus of ongoing debate. Some scholars argue for symmetry (SM). For example, a recent meta-analysis demonstrates equivalent levels of motivated partisan cognition across 51 experiments investigating the tendency to evaluate otherwise identical information more favorably when it supports versus challenges one's political beliefs or allegiances ([ 14 ][14]). In an illustrative experiment, liberals and conservatives viewed a film clip of a political demonstration in which protestors clashed with police. Despite viewing the identical clip, liberals rated the protesters as more violent when they believed it was an anti-abortion protest (a conservative cause) rather than a gay-rights protest (a liberal cause), whereas conservatives exhibited the opposite pattern (SM). Other scholars argue for asymmetry. For example, some evidence suggests that, relative to Democrats, Republicans have a higher need for order and greater trust in their gut-level intuitions. Such tendencies appear to motivate them to favor explanations that are straightforward and intuitive rather than complex and abstract, even when the latter types of explanation might be more accurate ([ 15 ][15]) (SM). Such findings are representative of the existing evidence, but conclusions remain tentative. Political sectarianism also undermines the core government function of competence—of providing for and protecting the people. Members of Congress increasingly prioritize partisan purity over the sorts of compromises that appeal to a large proportion of the population, a tendency that creates legislative gridlock. Issues that are not inherently partisan become politicized, impeding the ability to make progress on goals like mitigating climate change, reducing the federal debt, and safeguarding democratic rights. America's response to the coronavirus disease 2019 (COVID-19) pandemic highlights the perils of political sectarianism. An October 2019 report from Johns Hopkins University suggested that America was better prepared for a pandemic than any other nation (SM), but that report failed to account for the sort of political sectarianism that would, months later, make mask-wearing a partisan symbol, one favored more by Democrats than by Republicans. Democrat s were also more likely to prioritize stay-at-home orders despite their massive, immediate economic cost—a pattern that was especially prominent among highly sectarian partisans (SM). This schism, fomented in part by President Trump, pushed toward a disequilibrium in which too few people engaged sufficiently in commerce to stimulate economic growth while too few social-distanced sufficiently to contain the pandemic. The result has been lethal and expensive for Americans across the political spectrum. Political sectarianism is neither inevitable nor irreversible. When considering promising avenues for intervention, the goal is not to restore America to some halcyon republic of yore. As exemplified by the 1870s transition from the relatively antiracist Reconstruction era to the deeply racist Redemption era, many historic episodes of partisan comity rested upon bipartisan support for (or at least acquiescence to) antidemocratic institutions and behaviors, including the marginalization and disenfranchisement of women and racial minorities. The current divide is so potent in part because battles surrounding sexism and racism have grown strongly partisan. Rather, the goal of these interventions is to move toward a system in which the public forcefully debates political ideals and policies while resisting tendencies that undermine democracy and human rights. Given that substantial swaths of American society (including many who identify as Democrat or Republican) are fed up with surging sectarianism (SM), dedicated efforts to mitigate it may well land in fertile soil. Such efforts must circumvent the sectarian true believers, profiteers, and chaos-seekers who benefit from stoking sectarianism. These actors contribute directly to political sectarianism, and they leverage the government sclerosis caused by political sectarianism to derail efforts to address structural sources of that sectarianism, such as economic inequities and biased electoral procedures (SM). Nonetheless, scholars have begun to identify procedures that can potentially mitigate political sectarianism. These include efforts to help Americans comprehend opposing partisans regardless of their level of agreement, such as by focusing on commonalities rather than differences (e.g., “we're all Americans”; SM) or communicating in the moral language of the other side (e.g., when liberals frame the consequences of climate change in terms of sanctity violations; SM). Here, we consider three avenues for intervention that hold particular promise for ameliorating political sectarianism. The firs t addresses people's faulty perceptions or intuitions. For example, correcting misperceptions of opposing partisans, such as their level of hostility toward one's copartisans, reduces sectarianism ([ 5 ][7]) (SM ). Such correction efforts can encourage people to engage in cross-party interactions (SM) or to consider their own positive experiences with opposing partisans, especially a friend, family member, or neighbor. Doing so can reduce the role of motivated partisan reasoning in the formation of policy opinions (SM). A related idea is to instill intellectual humility, such as by asking people to explain policy preferences at a mechanistic level—for example, why do they favor their position on a national flat tax or on carbon emissions. According to a recent study, relative to people assigned to the more lawyerly approach of justifying their preexisting policy preferences, those asked to provide mechanistic explanations gain appreciation for the complexities involved (SM). Leaders of civic, religious, and media organizations committed to bridging divides can look to such strategies to reduce intellectual self-righteousness that can contribute to political sectarianism. A second avenue involves altering social-media platforms, although some popular ideas along these lines may be counterproductive. Echo chambers are widely blamed for surging sectarianism, but simply tweaking algorithms to show partisans more content from the opposition may aggravate sectarianism rather than reducing it ([ 7 ][9]). More promising are interventions that encourage people to deliberate about the accuracy of claims on social media, which causes them to evaluate the substance of arguments and reduces their likelihood of sharing false or hyperpartisan content ([ 12 ][16]) (SM). Another option is to use crowdsourcing to identify such content and the outlets that emit it, relying on users' ratings of trustworthiness to augment the efforts of professional fact-checkers. Such information can be incorporated into algorithmic rankings to reduce the presence of false or hyperpartisan content in people's news feeds (SM). A third avenue involves creating incentives for politicians and other elites to reduce their sectarianizing behaviors. People become less divided after observing politicians treating opposing partisans warmly, and nonpartisan statements from leaders can reduce violence. Campaign finance reform may help, especially by eliminating huge contributions from ideological extremists (SM). Reducing partisan gerrymandering likely would make representation fairer, generate more robust competition in the marketplace of political ideas, and send fewer extremists to the House of Representatives (SM). In 1950, the American Political Science Association issued a report expressing concern that America was insufficiently polarized, a perspective that remained dominant in the ensuing decades (SM). Ideological differentiation is an essential feature of party-based democracy, sharpening debates on important topics. Because most people lack the expertise required to make informed judgments on specific policies, divergent and internally coherent party platforms function as helpful heuristics that voters can use to prioritize their preferred policies and hold politicians accountable. But the ideological polarization the American Political Science Association had in mind has, in recent decades, been eclipsed among the public by political sectarianism. When politics becomes an identity-based struggle against depraved opponents—when ideals and policies matter less than dominating foes—government becomes dysfunctional. Viable political strategies focus less on policy-based arguments and more on marginalizing the opposition, with false smears and antidemocratic tactics if necessary. Insofar as politicians are pursuing unpopular policies, they are incentivized to destroy the idea of objectivity altogether, undermining the reputation of fact-checkers and mobilizing sectarian loyalists to believe “alternative facts.” As political sectarianism grows more extreme, pushing strong partisans deeper into congenial media enclaves that reinforce their narratives of moral righteousness, it may also become self-reinforcing, rendering mitigation efforts more difficult. Scholars have long argued that a shared threat can bring people together; indeed, some suggest that rising sectarianism in America is due in part to the loss of the Soviet Union as a unifying arch-nemesis. But such threats may do the opposite when sectarianism is extreme. COVID-19 offered a test case (SM). By the summer of 2020, 77% of Americans believed that the nation had grown more divided since the pandemic arrived that winter, a response 2.8 standard deviations higher than the mean of the 13 other nations in the study and 1.6 standard deviations higher than the second-highest nation (Spain). Such findings underscore the urgent need to counteract sectarianism before it grows more poisonous. Political sectarianism cripples a nation's ability to confront challenges. Bolstering the emphasis on political ideas rather than political adversaries is not a sufficient solution, but it is likely to be a major step in the right direction. The interventions proposed above offer some promising leads, but any serious effort will require multifaceted efforts to change leadership, media, and democratic systems in ways that are sensitive to human psychology. There are no silver bullets. [science.sciencemag.org/content/370/6516/533/suppl/DC1][17] 1. [↵][18]1. S. Iyengar, 2. Y. Lelkes, 3. M. 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J. Van Bavel, 2. A. Pereira , Trends Cogn. Sci. 22, 213 (2018). [OpenUrl][39] 11. [↵][40]1. M. H. Graham, 2. M. W. Svolik , Am. Polit. Sci. Rev. 114, 392 (2020). [OpenUrl][41] 12. [↵][42]1. G. Pennycook, 2. J. McPhetres, 3. Y. Zhang, 4. J. G. Lu, 5. D. G. Rand , Psychol. Sci. 31, 770 (2020). [OpenUrl][43] 13. [↵][44]1. L. Boxell et al ., “Cross-country trends in affective polarization (no. w26669),” National Bureau of Economic Research; [www.nber.org/papers/w26669][45] (2020). 14. [↵][46]1. P. H. Ditto et al ., Perspect. Psychol. Sci. 14, 273 (2019). [OpenUrl][47] 15. [↵][48]1. J. Baron, 2. J. T. Jost , Perspect. Psychol. Sci. 14, 292 (2019). [OpenUrl][49] Acknowledgments: We thank the Kellogg School of Management's Dispute Resolution Research Center and the Institute for Policy Research, both at Northwestern University. We thank S. Matz and A. Wilson for feedback on an earlier draft and T. Brader, D. Costanzo, M. DeBell, L. Harbridge-Yong, E. Groenendyk, M. Levendusky, and S. Westwood for responding to questions. 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The 2020 Formula 1 is finally set to get underway in Austria from Friday, four months after the intended start of what had been a hugely-anticipated season was delayed.


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Lewis Hamilton has joined Michael Schumacher as a seven-time world champion after securing the title at the Turkish Grand Prix.


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Lewis Hamilton made a powerful statement of intent as the Formula 1 season finally got under way at the Austrian Grand Prix.


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Website: bbc.co.uk
2020-11-06 17:31:56 UTC

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Several infectious diseases cause considerable mortality worldwide each year: Tuberculosis causes ∼1.2 million deaths, diarrheal disease causes ∼1.5 million deaths, and lower respiratory infections cause ∼700,000 deaths in children under 5 years old ([ 1 ][1]). Yet the scale and speed of innovation in developing tools for coronavirus disease 2019 (COVID-19) dwarf the development of those for global infectious diseases, which disproportionally affect resource-limited countries. By August 2020, ∼175 therapeutics and vaccines were in clinical trials for COVID-19 ([ 2 ][2]). By contrast, for 41 global infectious diseases or disease groups, only ∼250 therapeutics and vaccines were in clinical trials in August 2019 ([ 3 ][3]). A robust product pipeline and abridged development time frame for COVID-19 has primarily been enabled by three factors: scientific advances, operational efficiencies, and large-scale at-risk financing. A clear, well-financed path from research through product procurement now exists for COVID-19, shortening timelines while increasing output. This could underpin an approach for global infectious diseases. Recent scientific advances have revolutionized platform technologies and expanded the ability to rapidly identify therapeutic and vaccine candidates. High-throughput computational screening of molecular libraries against key pathogens and/or host targets has accelerated the ability to repurpose agents and identify entities against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, which causes COVID-19) ([ 4 ][4]). Candidate compounds with existing clinical safety data quickly entered clinical trials, leading to the repurposing of dexamethasone and remdesivir to treat hospitalized COVID-19 patients. Monoclonal antibodies (mAbs) can potentially provide near-immediate therapy and/or prophylaxis by bypassing the need for a host-generated immune response ([ 5 ][5]), and at lower costs and higher volumes than previously assumed. Vaccines have benefited from innovations in vector modalities, manufacturing, antigen design, computational biology, protein engineering, and gene synthesis ([ 6 ][6]). Such innovations may provide the technological basis for targeting other global infectious diseases. In response to COVID-19, the public health and regulatory communities are streamlining clinical development. Independently funded, designed, and conducted platform clinical trials, such as Accelerating COVID-19 Therapeutic Interventions and Vaccines (ACTIV), are structured under a single, adaptive “master” protocol to allow for continuous and consistent evaluation of multiple drug candidates, adding products as they become available and removing candidates as they are deemed futile. They also provide access to large, geographically diverse populations, and some have created or expanded operational structures in resource-limited countries ([ 7 ][7]). Timelines have been shortened because of accelerated regulatory reviews, flexible requirements to enter first-in-human trials, newer approaches to modeling population-specific issues, early approval mechanisms, and enhanced regulatory harmonization among countries ([ 8 ][8]). This increased efficiency in clinical trial execution and regulatory processes could be applied to other global infectious diseases. Historically, investment in product development for global infectious diseases has been restricted owing to the lack of financial returns compared to more profitable areas of drug development, such as oncology. However, the threat that pandemic human coronaviruses (HCoVs) pose to the global economy, political stability, and people's lives has stimulated the private sector, public sector, and philanthropic groups to devote considerable financial and human resources to product development. Previous HCoV outbreaks led to initial development activities that were accelerated with COVID-19. Supplementing these efforts, the U.S. government has provided over $10 billion for COVID-19 therapeutics and vaccines. Other governments, including the European Union, United Kingdom, Germany, and Canada, are making substantial financial commitments, as are large funding institutions ([ 2 ][2]). A fundamental principle behind this unprecedented funding is that financing for the entire product development process is made by the time a candidate enters early-stage clinical trials ([ 9 ][9]). This approach has mitigated the range of risks faced by different categories of developers (e.g., academia, nonprofit organizations, public-private partnerships, small biotechnology companies, and large multinational pharmaceutical companies) who may individually have widely varying risk-reward calculations. As a result, developers can simultaneously prepare for late-stage clinical trials, implement scaling up of manufacturing processes, and obtain advanced purchase commitments of large-scale supply—all during first-in-human clinical trials ([ 9 ][9]). Together, providing the full range of financing as early as possible in the product development process, articulating the need for multiple products, and acknowledging implicit failure of some candidates and platforms have overcome product development barriers. The result has been an extraordinary scale of therapeutic and vaccine development in the shortest time possible. A similar product development framework could be created for global infectious diseases. Such a framework could attempt to resolve three long-standing challenges for these diseases: the lack of interest in developing products, resulting in a diminished initial pipeline of candidates; the large pipeline attrition points between preclinical activities and early-stage clinical trials and between early- and late-stage clinical trials ([ 10 ][10]) that occur because of the considerable increases in development costs of these two transition points; and the extended timelines for product development. If these challenges are addressed, a more robust initial pipeline could be created, more candidates could advance to early- and late-stage clinical trials, and more products could be approved in a shorter period. A robust pipeline for global infectious diseases should include repurposed agents, mAbs, new chemical entities, and vaccines. Each of these categories possess strengths and limitations; thus, each may not prove beneficial for every disease. Repurposed agents may have existing preclinical data and clinical safety experience, putting them on the fastest development timelines. mAbs targeting proteins encoded by highly conserved regions of a pathogen's genome—thereby minimizing escape mutations and maximizing strain coverage—can be isolated from patients and modified to enhance their activities, for example, to extend half-life and induce host immune responses. New chemical entities could target families of pathogens to create “one-drug-multiple-bug” approaches to replace “one-drug-one-bug” approaches. Traditional vaccine platforms have a history of clinical validation and scaled production capacity. Emerging nucleic acid–based vaccine systems have promise for generating a candidate upon availability of a genomic sequence. Several factors must be considered to rapidly build and advance such a pipeline. Arguably the most critical factor is to incentivize all development groups and encourage aggressive competition. Public sector and philanthropic financing should address the cost of research, clinical trials, manufacturing, and supply agreements, and such financing should be available at the earliest possible part of the product development process. This is essential to overcome developers' decision to avoid product development because of lack of a clear revenue model. This financing, in turn, could stimulate the levels of investment and activity from the private sector observed in COVID-19, including public-private partnerships to advance candidates. A fundamental biological understanding of coronaviruses existed prior to COVID-19 and is necessary to drive product development, but a similar biological understanding needs to be improved for many global infectious diseases ([ 11 ][11]). While under development for COVID-19, predictive, validated preclinical assays, animal models, and human challenge models for infectious diseases would provide faster, cost-efficient methods to eliminate candidates earlier in the development cycle ([ 12 ][12], [ 13 ][13]). Moreover, implementing high-quality, decentralized clinical trials and using existing clinical trial networks could reduce the need for each developer to create complex multicountry clinical trial processes and infrastructure while still maintaining consistent evaluation methods ([ 14 ][14]). Machine learning could help optimize clinical trial design and identify populations most likely to benefit from a candidate, thereby reducing the large sample sizes currently required for late-stage clinical trials ([ 15 ][15]). Consideration should be given to what accelerated and flexible regulatory processes may be adopted from COVID-19, and which regulatory agencies should serve as benchmark approvals for those diseases that predominantly affect resource-limited settings. The manufacturing supply chain may need to be improved for some technologies facing global constraints. Additionally, access, affordability, and availability will need to be addressed to ensure that innovations reach the populations in greatest need. Implementing this strategy is not without risk, and there are challenges to overcome. Development of predictive models and biomarkers has proved difficult with COVID-19. The risk-benefit assessment for accelerated first-in-human testing during an unfolding pandemic may differ compared to that for endemic pathogens. Global capacity for late-stage clinical trials may initially be reached quickly in resource-limited settings. As seen with hydroxychloroquine, early approvals based on limited evidence can occur with compounds that ultimately demonstrate no benefit. The advanced financing available for COVID-19 candidates partially emerged from country-specific interests and, if repeated, may continue to foster inequitable access to new tools globally. Ultimately, the SARS-CoV-2 product development model may need optimization to realistically achieve success across multiple global infectious diseases. Of the ∼250 therapeutics and vaccines in clinical development for global infectious diseases, ∼30% are for HIV and AIDS ([ 3 ][3]). The innovation in antiretroviral medicines was initially sparked by strong political will coupled with streamlined regulatory processes. Growing demand produced attractive returns from resource-wealthy countries. By contrast, the distinct regulatory pathways and government funding to address the growing problem of resistance to antimicrobial agents (such as antibiotics) could not overcome the lack of a revenue model, thereby bankrupting companies that successfully developed safe and efficacious therapies and curtailing development activities. For the recent outbreak of Zika virus beginning in 2015 in the Americas, the time frame from identification of genomic sequences to advancing a nucleic acid vaccine into phase 1 clinical trials occurred within 4 months; but the threat to high-income countries quickly subsided, resulting in stalled product development programs. After nearly 40 years of continuous outbreaks in Africa, the potential global spread of Ebola became evident during the 2014–2016 outbreak and spurred public-private partnerships that recently achieved approval of two vaccines and one therapeutic mAb combination (with a second, single therapeutic mAb under regulatory review). Resource-limited countries are experiencing combined morbidity and mortality impacts from COVID-19: from the disease itself and from other global infectious diseases, owing, in large part, to diversion of resources. Which candidates in clinical trials for COVID-19 will reach regulatory approval, what limitations may come with licensed candidates, and the success of emerging technology platforms are all unknown. However, COVID-19 forced the world to construct a new product development approach, taking what was previously perceived as impossible and turning it into reality. How to implement this approach to address other global infectious diseases that continue to curtail global economic growth and devastate humanity must now be decided. 1. [↵][16]1. Institute for Health Metrics and Evaluation , Global Burden of Disease Study 2019; . 2. [↵][17]1. Policy Cures Research , COVID-19 R&D Tracker Update: 6 August 2020; . 3. [↵][18]1. Policy Cures Research , Neglected Diseases R&D Pipeline Tracker—August 2019; . 4. [↵][19]1. D. E. Gordon et al ., Nature 583, 459 (2020). [OpenUrl][20][CrossRef][21][PubMed][22] 5. [↵][23]1. M. Marovich, 2. J. R. Mascola, 3. M. S. Cohen , JAMA 324, 131 (2020). [OpenUrl][24][CrossRef][25][PubMed][26] 6. [↵][27]1. B. S. Graham , Science 368, 945 (2020). [OpenUrl][28][Abstract/FREE Full Text][29] 7. [↵][30]1. L. Corey, 2. J. R. Mascola, 3. A. S. Fauci, 4. F. S. Collins , Science 368, 948 (2020). [OpenUrl][31][Abstract/FREE Full Text][32] 8. [↵][33]1. J. L. Wilson et al ., Sci. Transl. Med. 12, eaax2550 (2020). 9. [↵][34]1. M. Slaoui, 2. M. Hepburn, , N. Engl. J. Med. 383, 1701 (2020). [OpenUrl][35] 10. [↵][36]1. R. Rappuoli, 2. S. Black, 3. D. E. Bloom , Sci. Transl. Med. 11, eaaw2888 (2019). [OpenUrl][37][FREE Full Text][38] 11. [↵][39]1. M. De Rycker, 2. B. Baragaña, 3. S. L. Duce, 4. I. H. Gilbert , Nature 559, 498 (2018). [OpenUrl][40][CrossRef][41] 12. [↵][42]1. J. Cohen , Science 368, 221 (2020). [OpenUrl][43][Abstract/FREE Full Text][44] 13. [↵][45]1. N. Eyal, 2. M. Lipsitch, 3. P. G. Smith , J. Infect. Dis. 221, 1752 (2020). [OpenUrl][46][PubMed][22] 14. [↵][47]1. COVID-19 Clinical Research Coalition , Lancet 395, 1322 (2020). [OpenUrl][48][PubMed][22] 15. [↵][49]1. W. R. Zame et al ., Stat. Biopharm. Res. 10.1080/19466315.2020.1797867 (2020). Acknowledgments: Thanks to D. Gollaher, B. Hubby, M. Kamarck, I. Pleasure, S. Shome, H. W. Virgin, C. Wells, and G. Yamey for their insightful comments. R.G. is an employee and owns shares of Vir Biotechnology, Inc. The author's opinions expressed in this article do not necessarily reflect Vir's official policy. 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Engagement score
1.18k

Honda Global | Honda to Conclude Participation in FIA Formula One World Championship


Engagement score
1.05k
Website: bbc.co.uk
2020-11-06 17:31:56 UTC

Formula 1 could still hold a world championship this year even if the season cannot start until October, managing director Ross Brawn says.


Engagement score
860

Diets rich in sugar, salt, and fat alter taste perception and food preference, contributing to obesity and metabolic disorders, but the molecular mechanisms through which this occurs are unknown. Here, we show that in response to a high sugar diet, the epigenetic regulator Polycomb Repressive Complex 2.1 (PRC2.1) persistently reprograms the sensory neurons of Drosophila melanogaster flies to reduce sweet sensation and promote obesity. In animals fed high sugar, the binding of PRC2.1 to the chromatin of the sweet gustatory neurons is redistributed to repress a developmental transcriptional network that modulates the responsiveness of these cells to sweet stimuli, reducing sweet sensation. Half of these transcriptional changes persist despite returning the animals to a control diet, causing a permanent decrease in sweet taste. Our results uncover a new epigenetic mechanism that, in response to the dietary environment, regulates neural plasticity and feeding behavior to promote obesity.


Engagement score
853

> Science's COVID-19 reporting is supported by the Pulitzer Center and the Heising-Simons Foundation October was a good month for Gilead Sciences, the giant U.S. manufacturer of antivirals. On 8 October, the company inked an agreement to supply the European Union with its drug remdesivir as a treatment for COVID-19—a deal potentially worth more than $1 billion. Two weeks later, on 22 October, remdesivir became the first COVID-19 drug approved by the U.S. Food and Drug Administration (FDA). The decisions mean Gilead can cash in big in two major markets, both with soaring COVID-19 cases. But they baffled scientists who have closely watched the clinical trials of remdesivir unfold over the past 6 months—and who have many questions about its worth. At best, one large, well-designed study found that remdesivir, which must be infused intravenously, modestly reduced the time to recover from COVID-19 in hospitalized patients with severe illness. A few smaller studies found no impact on the disease whatsoever, and none has found that the antiviral reduces patients' level of SARS-CoV-2, the causative virus. Then, on 15 October, the fourth and largest study delivered what some believed was a coup de grâce: The World Health Organization's (WHO's) giant Solidarity trial showed that remdesivir does not reduce mortality or the time COVID-19 patients take to recover. Science has learned that both FDA's decision and the EU deal came about under unusual circumstances that gave the company important advantages. FDA never consulted a group of outside experts that it has at the ready to weigh in on complicated antiviral drug issues. FDA can tap that group, the Antimicrobial Drugs Advisory Committee (AMDAC), to review all available data on experimental treatments and then make recommendations about drug approvals—yet it has not convened once during the pandemic. The EU, meanwhile, agreed to the remdesivir purchase price exactly 1 week before the disappointing Solidarity trial results came out. It was unaware of those results, but Gilead knew the trial was a bust; it had begun to review the data on 23 September. “This is a very, very bad look for the FDA, and the dealings between Gilead and EU make it another layer of badness,” says Eric Topol, a cardiologist at the Scripps Research Translational Institute. FDA has no obligation to convene the panel for its decisions, stresses AMDAC member David Hardy, an HIV/AIDS scientist of the University of California, Los Angeles. Yet Hardy is “amazed” the agency didn't consult it in this case. “This sets the standard for the first COVID-19 antiviral,” he says. “That really is something that's very, very important.” FDA did not respond to Science 's request to discuss why it opted against convening the committee, noting only that it is “at the discretion” of division directors. But FDA's inaction stands in sharp contrast to its handling of COVID-19 vaccines; it convened an advisory group to discuss potential dilemmas the very day of the remdesivir approval. Gilead, for its part, acknowledges it had seen an early draft of the Solidarity results before signing the EU deal. But Gilead has aggressively challenged the validity of the data, in part because the study was done in countries with widely varying health care standards. That criticism has angered Solidarity investigators. Half the patients who received remdesivir were treated in Europe and Canada, WHO notes, and the others were not necessarily in countries with substandard health care. “It's appalling to see how Gilead tries to badmouth the Solidarity trial,” says Marie-Paule Kieny, director of research at the French medical research agency INSERM and a former WHO officer. On 10 January, 2 days after China revealed SARS-CoV-2 causes COVID-19, researchers published an encouraging study in Nature Communications about remdesivir, originally developed to fight the Ebola and hepatitis C viruses. In both test tube and mouse studies, it had powerful inhibitory effects on a SARS-CoV-2 relative that causes Middle East respiratory syndrome. Two weeks later, doctors treated the first confirmed U.S. case with the drug and reported the 35-year-old man improved rapidly. An interim analysis from a large-scale clinical trial by the National Institutes of Health (NIH), announced on 29 April, showed the drug reduced the median recovery time of severely ill, hospitalized COVID-19 patients from 15 days to 11 days. A second study, in China, appeared the same day and found no statistically significant benefit, however. Two days later, FDA granted an emergency use authorization (EUA) that allowed the drug to be given for severe COVID-19, a move President Donald Trump praised in an Oval Office press event with Daniel O'Day, CEO of Gilead. But the mixed messages about the drug continued: In August, a Gilead-sponsored study showed patients with moderate pneumonia treated for 5 days with remdesivir improved more quickly than those who received standard care, but oddly, those treated for 10 days did not. Nevertheless, shortly afterward, FDA expanded remdesivir's EUA to include all hospitalized COVID-19 patients. To Topol, FDA's move resembled heavily criticized EUAs issued earlier for the malaria drug hydroxychloroquine—which the agency later rescinded—and antibody-rich “convalescent” plasma. In an open letter to FDA Commissioner Stephen Hahn, he wrote: “These repeated breaches demonstrate your willingness to ignore the lack of scientific evidence, and to be complicit with the Trump Administration's politicization of America's healthcare institutions.” Many scientists expected WHO's Solidarity trial—which had 2750 patients on remdesivir, about three times as many as all other published trials put together—to resolve the drug's worth. Conducted in 30 countries, Solidarity compared remdesivir and three other repurposed drugs with each other and the standard of care. (Unlike the NIH and Chinese trials, it did not use a placebo.) None of the drugs lowered mortality among hospitalized patients, it found, and the investigators also noted that remdesivir did not affect “the duration of hospitalization” or whether COVID-19 patients required ventilators. Solidarity described the results to FDA representatives on 10 October and in a preprint posted 5 days later. But 1 week after that, FDA approved the drug, having reviewed data only from the NIH study and two Gilead-sponsored trials. It had ignored the Solidarity data as well as the findings in China. That infuriated the Solidarity team. “The mantra I've always heard as a joke about the FDA is that they say ‘In God we trust, everyone else has to provide data,’” Kieny says. “So look at all the data.” Gilead Chief Medical Officer Merdad Parsey argued in an open letter posted the day of FDA's remdesivir approval that Solidarity “does not negate other study results—particularly from a trial designed with the strictest of scientific standards,” like NIH's study. The company further noted that the Solidarity results have not been peer reviewed and told Science WHO had yet to provide Gilead “the underlying data sets or statistical analysis plan” for the trial. WHO says Gilead knew the analysis plan before joining the trial and will receive the full data set once the study is complete, and that FDA traditionally reviews all available data, including unpublished findings. Clifford Lane of the National Institute of Allergy and Infectious Diseases, who helped run the NIH study, says its main difference with Solidarity is “the degree of granularity” of the analyses of subgroups that may have benefited. “I think the Solidarity data are fine,” Lane says. “It's a very large study and it has a very robust endpoint.” Richard Peto, a University of Oxford statistician and epidemiologist who helped design Solidarity and analyze the data, stresses that the WHO trial cannot prove remdesivir has no benefit for COVID-19. “Gilead and the FDA have sort of maneuvered us into a position where we're being asked to try and prove remdesivir does nothing rather than asking the usual way round, which is, ‘Can the manufacturers prove it does something?’” It's still possible that remdesivir might help people at early stages of disease, says Martin Landray of Oxford, who is co-leading the world's largest study of various COVID-19 treatments. But it “definitely doesn't work in the sickest patients where the biggest gains would be.” Treating patients earlier comes at a price. “You won't save many lives, and you'll have to treat a lot of patients,” he says. “And it'll cost you a fortune.” ![Figure][1] GRAPHIC: C. BICKEL/ SCIENCE At the same time, the trials have not ruled out the possibility of harmful side effects. In late August, WHO noted a disproportionately high number of reports of liver and kidney problems in patients on remdesivir. And the European Medicines Agency (EMA) said last month that its safety committee had begun to assess reports of acute kidney injuries in some patients taking the drug. To many scientists, such complexities underscore that FDA should have consulted AMDAC, its panel of outside experts, for a vigorous debate. It could have “elevated the discussion,” says AMDAC Chair Lindsey Baden, an infectious disease specialist at Brigham and Women's Hospital. “Hydroxychloroquine, convalescent plasma, remdesivir—these are complicated decisions given the imperfect nature of the data. … The urgency of the clinical use gives all the more reasons to have an open discussion,” says Baden, whose group last met in October 2019. EMA, Europe's FDA counterpart, in July gave “conditional approval” to remdesivir—similar to an EUA—but it has yet to give its full blessing. The European Union nevertheless has negotiated a “joint procurement agreement” with Gilead, signed on 8 October, that secures as many as 500,000 treatment courses for $1.2 billion. A spokesperson for the European Commission confirms to Science it was not informed of the drug's failure in the Solidarity trial until the next day: “There was no discussion with WHO about the ongoing study prior to signing the contract.” When Science asked Gilead why it didn't disclose the Solidarity data during the negotiations, the company said the draft manuscript it received from WHO in late September was “heavily redacted.” WHO says the only information blacked out was results relating to the other drugs used in the trial because of confidentiality agreements. Although the agreement with Gilead locks EU members into a price of about $2400 for a full course of remdesivir, it does not obligate any countries to purchase the drug, the Commission spokesperson says. But Yannis Natsis of the nonprofit European Public Health Alliance says that given the Solidarity results, the European Union “should at least renegotiate the volume of the doses and the price.” To Kieny, this investment in a drug that may help just a few patients is an “enormous” waste. “You can always say, ‘OK, now, if I disaggregate the population and if I take only those who have a blue eye and a wooden leg, maybe this is very effective,’” she says. On 28 October, Gilead told investors that remdesivir has brought in $873 million so far this year. “We're proud to be at the front end of this with a very potent antiviral,” O'Day said. [1]: pending:yes


Engagement score
852

George Russell believes speculation about his Formula 1 future with Williams has been "fed by the Perez camp", and expects clarity about his position from the team within a week


Engagement score
803

Two archaic lineages overlapped with modern humans outside of Africa: the well-studied Neanderthals and their more mysterious cousins, the Denisovans. Denisovan remains are rare, being limited to Denisovan Cave in Siberia and a putative, undated jaw from Tibet. However, there is evidence for multiple introgressions from Denisovans into modern-day humans, especially in Australasian populations. By examining the sediment of Baishiya Karst Cave located on a high plateau in Tibet, Zhang et al. identified ancient mitochondrial DNA from Denisovans indicating their presence at about 100 thousand, 60 thousand, and possibly 45 thousand years ago. This finding provides insight into the timing and distribution of Denisovans in Asia and extends the time of occupation of the Tibetan plateau by hominins. Science , this issue p. [584][1] A late Middle Pleistocene mandible from Baishiya Karst Cave (BKC) on the Tibetan Plateau has been inferred to be from a Denisovan, an Asian hominin related to Neanderthals, on the basis of an amino acid substitution in its collagen. Here we describe the stratigraphy, chronology, and mitochondrial DNA extracted from the sediments in BKC. We recover Denisovan mitochondrial DNA from sediments deposited ~100 thousand and ~60 thousand years ago (ka) and possibly as recently as ~45 ka. The long-term occupation of BKC by Denisovans suggests that they may have adapted to life at high altitudes and may have contributed such adaptations to modern humans on the Tibetan Plateau. [1]: /lookup/doi/10.1126/science.abb6320


Engagement score
758

Arthropod herbivores cause substantial economic costs that drive an increasing need to develop environmentally sustainable approaches to herbivore control. Increasing plant diversity is expected to limit herbivory by altering plant-herbivore and predator-herbivore interactions, but the simultaneous influence of these interactions on herbivore impacts remains unexplored. We compiled 487 arthropod food webs in two long-running grassland biodiversity experiments in Europe and North America to investigate whether and how increasing plant diversity can reduce the impacts of herbivores on plants. We show that plants lose just under half as much energy to arthropod herbivores when in high-diversity mixtures versus monocultures and reveal that plant diversity decreases effects of herbivores on plants by simultaneously benefiting predators and reducing average herbivore food quality. These findings demonstrate that conserving plant diversity is crucial for maintaining interactions in food webs that provide natural control of herbivore pests.


Engagement score
716

In the round-up: Steiner didn't want to give drivers "stupid presents" as parting gifts • Opmeer victorious in F1 Esports • GT World Challenge calendar confirmed


Engagement score
625

Ferrari's Sebastian Vettel says F1 faces 'big challenges' to secure its future in the context of the world's environmental problems.


Engagement score
588

Valtteri Bottas maintained his position at the head of the timesheet on F1's Portimao debut but the battle for the top positions in the second practice session was overshadowed by a collision between Max Verstappen and Lance Stroll and a car fire for Pierre Gasly.


Engagement score
587

MotoGP: The Portuguese government has declared that every event organized will be re-assessed. In the F1, 14 positive cases were registered amont the teams after the Portugal GP


Engagement score
580

Toto Wolff has revealed a radio failure led to the tyre mix-up that cost George Russell a likely maiden Formula 1 victory in Sunday's Sakhir Grand Prix.


Engagement score
578

190 races. That’s how long Sergio Perez had to wait - the longest wait in F1 history - to finally taste the winner's champagne in Formula 1, the Mexican taking his maiden victory the hard way after a breathless and dramatic Grand Prix in Sakhir.


Engagement score
541

Renault CEO Luca de Meo is installing a spirit inside the Formula 1 squad that has similarities to the story behind the 'Ford v Ferrari' movie, reckons team boss Cyril Abiteboul.


Engagement score
430

Ferrari is now in favour of a Formula 1 engine development freeze from 2022 after agreeing to bring forward the introduction of the new power units to 2025.


Engagement score
393

Global biodiversity policy is at a crossroads. Recent global assessments of living nature ([ 1 ][1], [ 2 ][2]) and climate ([ 3 ][3]) show worsening trends and a rapidly narrowing window for action. The Convention on Biological Diversity (CBD) has recently announced that none of the 20 Aichi targets for biodiversity it set in 2010 has been reached and only six have been partially achieved ([ 4 ][4]). Against this backdrop, nations are now negotiating the next generation of the CBD's global goals [see supplementary materials (SM)], due for adoption in 2021, which will frame actions of governments and other actors for decades to come. In response to the goals proposed in the draft post-2020 Global Biodiversity Framework (GBF) made public by the CBD ([ 5 ][5]), we urge negotiators to consider three points that are critical if the agreed goals are to stabilize or reverse nature's decline. First, multiple goals are required because of nature's complexity, with different facets—genes, populations, species, deep evolutionary history, ecosystems, and their contributions to people—having markedly different geographic distributions and responses to human drivers. Second, interlinkages among these facets mean that goals must be defined and developed holistically rather than in isolation, with potential to advance multiple goals simultaneously and minimize trade-offs between them. Third, only the highest level of ambition in setting each goal, and implementing all goals in an integrated manner, will give a realistic chance of stopping—and beginning to reverse—biodiversity loss by 2050. Achieving this will require prompt and concerted measures to address the causes of biodiversity loss ([ 6 ][6]), meaning that implementation will be crucial. The draft GBF ([ 5 ][5]) has advanced conceptually relative to its predecessor by highlighting the importance of outcome-oriented goals (i.e., what we want the state of nature to be in 2050 in terms of, for example, species extinction rates or ecosystem area and integrity ). These outcome goals link the broad aspirational vision (“living in harmony with nature”; see SM) to the concrete actions needed to achieve it. The outcome goals—operationalized by more specific targets and assessed using indicators—provide a compass for directing actions and a way of checking their results; for example, whether meeting a set of action-based targets (e.g., designating X% of Earth's surface as protected areas) delivers on a desired outcome (e.g., “no net loss in the area and integrity of natural ecosystems” ) needed to realize the aspirational vision. It is more important than ever that the necessary outcomes are incorporated in the GBF and that they adequately cover the distinct facets of nature, are sufficiently ambitious, and are grounded in the best knowledge available. Various proposals for the new CBD outcome goals have focused on individual facets of nature, such as ecosystems ([ 7 ][7]), species ([ 8 ][8]), or genetic diversity ([ 9 ][9]). What has been missing is a unified view on how these facets relate to each other in setting goals to achieve the CBD's 2050 vision. To address this gap, we surveyed, evaluated, and discussed published proposals of goals for ecosystems, species, genetic diversity, and nature's contributions to people (NCP) in relation to the empirical and theoretical knowledge in the scientific literature. Our evaluation addresses whether proposed goals encompass, are consistent with, or are opposed to each other; whether they are sufficiently ambitious such that meeting them will indeed curb and reverse biodiversity trends; and whether they contain all the elements needed to make them difficult to “game” (i.e., avoid making substantial contributions by exploiting weaknesses in wording) (see SM for details on our analysis). As the failure to achieve the CBD's single 2010 goal—to substantially reduce the rate of biodiversity loss—shows, having an “apex” goal does not guarantee success. Whereas the mission of the United Nations Framework Convention on Climate Change (UNFCCC) focuses on one main outcome—preventing dangerous climate change, for which one goal and indicator (well below 2°C) provide a reasonable proxy for the others—CBD's vision and mission have three components that are distinct, complementary, and often trade off with each other: conserving nature, using it sustainably, and (though we do not consider this component here) sharing its benefits equitably. The nature conservation component is itself complex because biodiversity includes variation in life at all levels, from genes to ecosystems. Recognizing this, the proposed formulation of the GBF ([ 5 ][5]) (see SM) started by proposing separate goals that explicitly covered ecosystems, species, genetic diversity, and the contributions to people derived from them. Whether this structure is retained, or the necessary outcomes for these facets are instead subsumed into more overarching goals, our analysis (see SM) shows that all these facets need to be addressed explicitly because of how they interrelate. If the facets were nested into one another like Russian dolls, or at least nearly so, then a single concise goal that specifies one number about the most encompassing facet could cover all of them. However, although the facets of nature are deeply interlinked, they are far from neatly nested and represent instead a “minimum set” ([ 10 ][10], [ 11 ][11]). As a result, there is no single goal based on any one facet that would, if realized, guarantee by itself that the necessary outcome for the other facets would be achieved ([ 12 ][12], [ 13 ][13]). Another reason for having multiple goals is “Goodhart's law”: Whenever a measure becomes a policy goal itself, it ceases to be a good measure of the true state of the system because it can be “gamed” ([ 14 ][14]). For example, incentives would favor actions to enhance the targeted metric irrespective of effects on the rest of nature. Given nature's multidimensionality, this approach would cause inefficient use of resources at best and possibly promote perverse outcomes ([ 14 ][14]). If the CBD enshrined an “apex” goal focusing on a single facet of nature, other facets may be relegated to the back seat. By incentivizing holistic actions, a framework with multiple goals reduces the risk that the goals could be achieved without also achieving the overarching vision that they were intended to serve. ![Figure][15] Sustainability at the crossroads Columns show different facets of nature and their contributions to people (NCP). Each cell shows a potential goal (in bold) at a particular level of ambition in attaining it and some consequences of reaching it, including effects on the other facets of nature and NCP. Only the scenario in green would contribute substantially to “bending the curve” of biodiversity loss. See supplementary materials for further details. The interdependence of ecosystems, species, genetic diversity, and NCP offers the opportunity to design policies and actions that contribute to multiple goals simultaneously. This offers the possibility for mutually reinforcing goals, in which progress toward one goal also advances the others, even though each facet of nature will also require targeted actions to address its specificities (see SM). For example, restoring ecosystems that are species-rich, have many endemics, and store large amounts of carbon, such as tropical peatlands, contributes toward all goals. The downside of this interdependence is that failure to achieve one goal will likely undermine others in a negative mutually reinforcing cycle: Ongoing loss of area and integrity of tropical peatlands leads to global extinctions and reduces options for climate mitigation; climate change then causes further loss of ecosystems, species, populations, genetic diversity, and NCP (see SM). Although the scientific and management communities have been long aware of interactions among biodiversity goals and targets, these linkages have not been sufficiently operationalized ([ 11 ][11]). We highlight the need for the connectedness, partial dependence, and imperfect nesting of nature's facets to be built right from the start in the design of outcome goals, targets, indicators, and actions. In addition to addressing different facets of nature, goals must be set across the whole gradient from “natural” to “managed” ecosystems, attending to the specificities of these different landscapes (see SM). Holistically designed goals on ecosystems, species, genetic diversity, and NCP are necessary to achieve the 2050 vision; whether they are sufficient will depend on the level of ambition that these goals reflect. Even perfect implementation cannot make up for outcome goals set too low or too narrowly at the start. Different levels of ambition are, for example, whether the curve of biodiversity loss will bend (high ambition) or merely flatten (low), or whether no net loss of ecosystems is specified with a lax (low) or strict (high) criterion for replaceability (see SM). The interdependence among facets of nature means that missing a goal for one facet risks also missing goals related to other facets, whereas achieving each goal at a sufficient ambition level can contribute to reaching the others. Our synthesis of the evidence (see the figure, and SM) illustrates that the CBD's 2050 vision is feasible only by aiming high with each of the goals. Lower levels of ambition will deliver inadequate outcomes, including loss in area and integrity of ecosystems, more global extinctions, reduced abundance and performance of many important species, loss of genetic diversity, and reduced benefits to people. This would not only compromise the objectives of the CBD but also undermine progress toward most of the United Nations Sustainable Development Goals and the Paris Climate Agreement ([ 1 ][1]). The stakes are high. Our arguments for setting multiple goals do not mean that there is no place for a compelling and unifying overarching vision. Collective action over more than a century offers a clear lesson: To gain political traction, any unifying vision needs to be a rallying cry—broad, normative, inspirational, and aspirational. The CBD process has already set such clear vision: “living in harmony with nature.” The goals underpinning the vision, by contrast, need to be unambiguous and strongly based on the best available knowledge to make it possible to derive SMART (specific, measurable, assignable, realistic, time-related) operational targets ([ 15 ][16]) from them. In sum, one compelling overarching vision, buttressed by facet-specific goals that are mutually reinforcing, scientifically tractable, and individually traceable, will deliver the overarching vision more reliably than any single-facet goal. Using a single-facet goal as the only flagship of global biodiversity policy is analogous to using blood pressure or body mass index as the sole surrogate for the vision of “vibrant health”: simple but risky. The main challenge ahead lies not in the number of goals but rather in making them happen. However many goals are in the GBF, their specific wording and the supporting framework of targets and indicators will be equally influential on global policy. This wording will be decided by the governments at the 15th Conference of the Parties (COP15) of the CBD in 2021. We summarize critical elements emerging from our analysis that we hope delegates will consider when establishing the GBF, intended to help maximize positive impacts of each goal and minimize perverse interpretations (see the box). ![Figure][15] Key considerations for 2050 biodiversity goals The following key elements are essential for the new post-2020 Convention on Biological Diversity goals. If not fully expressed in the actual goals, they should structure the action targets and indicator framework. To clarify their ambition and enable tracking of legitimate progress, all goals need to have clear reference years (e.g., 2020). For detailed explanations and supporting references, see supplementary materials. We have deliberately focused on how the different facets of nature and their contributions to people should look in 2030 and 2050 to achieve the CBD 2050 vision (with 2030 seen as reflecting crucial “stepping stones” in the right direction toward 2050). We have not evaluated the economic and political consequences of the proposed goals nor the governance and distributional challenges of their implementation. In the case of NCP, we focused on their generation rather than on how they are accessed to meet actual needs and therefore result (or not) in people's good quality of life. Implementing actions to achieve these outcomes without considering social and political issues would be a recipe for further failure. We thus provide just one piece of the formidable puzzle that must be resolved. But it is an essential piece: what could be effective from the biological perspective, provided that the right actions are implemented and all relevant actors are involved in pursuing them. Actions to implement these goals will need to tackle the indirect socioeconomic drivers (and underlying value systems) at the root of nature's decline as well as the direct proximal drivers on which conservation has mostly focused to date ([ 1 ][1]). Only then will the 2050 vision have a chance. We exhort the parties to be ambitious in setting their goals, and holistic in their actions afterward, to transition to a better and fairer future for all life on Earth. [science.sciencemag.org/content/370/6515/411/suppl/DC1][17] 1. [↵][18]1. S. Dèaz et al Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services (IPBES), “The global assessment report on biodiversity and ecosystem services: Summary for policymakers,” S. Dèaz et al., Eds. (IPBES secretariat, Bonn, 2019). 2. [↵][19]1. S. Díaz et al ., Science 366, eaax3100 (2019). [OpenUrl][20][Abstract/FREE Full Text][21] 3. [↵][22]1. A. 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We thank the following contributors to the Report to the CBD Synthesizing the Scientific Evidence to Inform the Development of the Post-2020 Global Framework on Biodiversity, on which this article builds: J. Bascompte, J. Cariño, N. Castañeda-Alvarez, M. Azeredo de Dornelas, S. Hoban, S. Jones, P. Jordano, L. Laikre, N. Maxted, P. Miloslavich, D. Moreno-Mateos, R. Ogden, G. Segelbacher, J.-C. Svenning. We also thank members of the Future Earth GRP EvolvES (formerly bioGENESIS): M. Bellon, L. Colli, F. Forest, M. Johnson, R. Kassen, C. Souffreau, and E. Vázquez-Domínguez. We thank D. Cooper for useful discussions and for advice in the design of the meeting. We thank Georgina M. Mace for discussions about this paper and countless others and for her wonderful and generous leadership, insight, support, and example over many years; we will miss her greatly. 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{openurl}?query=rft.jtitle%253DAnnu.%2BRev.%2BEnviron.%2BResour.%26rft.volume%253D37%26rft.spage%253D25%26rft_id%253Dinfo%253Adoi%252F10.1146%252Fannurev-environ-042911-093511%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [38]: /lookup/external-ref?access_num=10.1146/annurev-environ-042911-093511&link_type=DOI [39]: #xref-ref-11-1 "View reference 11 in text" [40]: {openurl}?query=rft.jtitle%253DBasic%2BAppl.%2BEcol.%26rft.volume%253D15%26rft.spage%253D633%26rft_id%253Dinfo%253Adoi%252F10.1016%252Fj.baae.2014.09.004%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [41]: /lookup/external-ref?access_num=10.1016/j.baae.2014.09.004&link_type=DOI [42]: #xref-ref-12-1 "View 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{openurl}?query=rft.jtitle%253DConserv.%2BLett.%26rft.volume%253D4%26rft.spage%253D264%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [48]: #xref-ref-15-1 "View reference 15 in text" [49]: {openurl}?query=rft.jtitle%253DConserv.%2BBiol.%26rft.volume%253D33%26rft.spage%253D1360%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx


Engagement score
379

Mercedes team principal Toto Wolff has cautioned against a “fuel and oil war” as Formula 1 continues its push for sustainability with the next set of power unit regulations.


Engagement score
322

Red Bull says Nico Hulkenberg could be an option for the team in 2021, after revealing that it even spoke to the German about driving at the Nurburgring.


Engagement score
318

The good news is that, at least for now, the Portimao MotoGP season finale is set to go ahead on November 20-22.The bad news is that plans to have around 30,000 fans present for the circuit's inaugural MotoGP round have now been blocked by the prime minister.Like many countries, Portugal is now battling to contain rising coronavirus cases but the final straw as far as fans being present for the MotoGP appears to have been a lack of social distancing among a similar number of F1 spectators at last month's four-wheel grand prix.“What happened at the [F1] Grand Prix is unacceptable and cannot be


Engagement score
313

Achieving a rapid global decarbonization to stabilize the climate critically depends on activating contagious and fast-spreading processes of social and technological change within the next few years. Drawing on expert elicitation, an expert workshop, and a review of literature, which provides a comprehensive analysis on this topic, we propose concrete interventions to induce positive social tipping dynamics and a rapid global transformation to carbon-neutral societies. These social tipping interventions comprise removing fossil-fuel subsidies and incentivizing decentralized energy generation, building carbon-neutral cities, divesting from assets linked to fossil fuels, revealing the moral implications of fossil fuels, strengthening climate education and engagement, and disclosing greenhouse gas emissions information.


Engagement score
310

Mercedes-Benz raise their stake in Aston Martin to 20%, offer the Stroll-owned company with their technology in exchange.


Engagement score
299

Two Formula 1 personnel have tested positive for coronavirus in the last week.


Engagement score
297

Formula 1 cars are currently faster than ever before, but they're also bigger than ever. F1 technical consultant Rob Smedley explains the reasons behind the increase in size


Engagement score
292

Mercedes boss Toto Wolff is of the opinion that a few teams like Ferrari could "write off" 2021, in order to focus on the 2022 season.


Engagement score
283

Free-to-air coverage of the 2021 Formula 1 world championship will be broadcast on Network 10 in 2021


Engagement score
265
Website: bbc.co.uk
2020-11-06 17:31:56 UTC

Formula 1 plans to create an isolated environment for competitors when it starts racing again in July.


Engagement score
255

A focus of battery research has been the development of a range of lithium, sodium, and potassium cathodes, but improving anode materials is also an important goal. Silicon has shown some promise for replacing graphite because of its exceptional capacity, but the dramatic volume change during lithiation-delithiation processes often leads to failure. Jin et al. developed a composite that is made of black phosphorous and graphite in its core and covered with swollen polyaniline. In contrast to previous efforts, bonding between the carbon and phosphorous allows for a high charging rate without sacrifices in capacity and cycling stability. Science , this issue p. [192][1] High-rate lithium (Li) ion batteries that can be charged in minutes and store enough energy for a 350-mile driving range are highly desired for all-electric vehicles. A high charging rate usually leads to sacrifices in capacity and cycling stability. We report use of black phosphorus (BP) as the active anode for high-rate, high-capacity Li storage. The formation of covalent bonds with graphitic carbon restrains edge reconstruction in layered BP particles to ensure open edges for fast Li+ entry; the coating of the covalently bonded BP-graphite particles with electrolyte-swollen polyaniline yields a stable solid–electrolyte interphase and inhibits the continuous growth of poorly conducting Li fluorides and carbonates to ensure efficient Li+ transport. The resultant composite anode demonstrates an excellent combination of capacity, rate, and cycling endurance. [1]: /lookup/doi/10.1126/science.aav5842


Engagement score
236

The British GT season is set for an epic Silverstone 500 climax this weekend with titles up for grabs and former F1 world champion Jenson Button part of a bumper field - and you can watch the championship's marquee race live on Sky Sports F1.


Engagement score
228

Andreas Seidl, Team Principal at McLaren, criticized the idea of holding 25 races in a season by reducing the race weekends to just two days.


Engagement score
217

According to reports, Russian billionaire Dmitry Mazepin believes the bidding process of the Force India F1 team buyout was 'flawed'.


Engagement score
197
Website: bbc.co.uk
2020-11-18 16:28:40 UTC

Formula 1 has named Turkey, Bahrain and Abu Dhabi as the three countries that will host four races to conclude the 2020 season.


Engagement score
195

Gerhard Berger's Ferrari years. The Austrian F1 veteran reveals what it takes to drive for the Maranello team


Engagement score
188

Who proved himself? Who is forever young? Who kept his eye in?


Engagement score
185
Website: nytimes.com
2020-11-14 15:48:59 UTC

The pandemic has forced the sport to patch together a schedule with new races and new tracks, with more to come. What’s the same is Mercedes, which is still on top.


Engagement score
172

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