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      Robust neutralizing antibodies to SARS-CoV-2 infection persist for months

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          SARS-CoV-2 antibodies persist

          As the number of daily COVID-19 cases continues to mount worldwide, the nature of the humoral immune response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains uncertain. Wajnberg et al. used a cohort of more than 30,000 infected individuals with mild to moderate COVID-19 symptoms to determine the robustness and longevity of the anti–SARS-CoV-2 antibody response. They found that neutralizing antibody titers against the SARS-CoV-2 spike protein persisted for at least 5 months after infection. Although continued monitoring of this cohort will be needed to confirm the longevity and potency of this response, these preliminary results suggest that the chance of reinfection may be lower than is currently feared.

          Science, this issue p. 1227

          Abstract

          Antibodies generated after mild to moderate SARS-CoV-2 infection are neutralizing and relatively stable for at least 5 months.

          Abstract

          Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a global pandemic with millions infected and more than 1 million fatalities. Questions regarding the robustness, functionality, and longevity of the antibody response to the virus remain unanswered. Here, on the basis of a dataset of 30,082 individuals screened at Mount Sinai Health System in New York City, we report that the vast majority of infected individuals with mild-to-moderate COVID-19 experience robust immunoglobulin G antibody responses against the viral spike protein. We also show that titers are relatively stable for at least a period of about 5 months and that anti-spike binding titers significantly correlate with neutralization of authentic SARS-CoV-2. Our data suggest that more than 90% of seroconverters make detectable neutralizing antibody responses. These titers remain relatively stable for several months after infection.

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          Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation

          Structure of the nCoV trimeric spike The World Health Organization has declared the outbreak of a novel coronavirus (2019-nCoV) to be a public health emergency of international concern. The virus binds to host cells through its trimeric spike glycoprotein, making this protein a key target for potential therapies and diagnostics. Wrapp et al. determined a 3.5-angstrom-resolution structure of the 2019-nCoV trimeric spike protein by cryo–electron microscopy. Using biophysical assays, the authors show that this protein binds at least 10 times more tightly than the corresponding spike protein of severe acute respiratory syndrome (SARS)–CoV to their common host cell receptor. They also tested three antibodies known to bind to the SARS-CoV spike protein but did not detect binding to the 2019-nCoV spike protein. These studies provide valuable information to guide the development of medical counter-measures for 2019-nCoV. Science, this issue p. 1260
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            Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses

            Over the past 20 years, several coronaviruses have crossed the species barrier into humans, causing outbreaks of severe, and often fatal, respiratory illness. Since SARS-CoV was first identified in animal markets, global viromics projects have discovered thousands of coronavirus sequences in diverse animals and geographic regions. Unfortunately, there are few tools available to functionally test these viruses for their ability to infect humans, which has severely hampered efforts to predict the next zoonotic viral outbreak. Here, we developed an approach to rapidly screen lineage B betacoronaviruses, such as SARS-CoV and the recent SARS-CoV-2, for receptor usage and their ability to infect cell types from different species. We show that host protease processing during viral entry is a significant barrier for several lineage B viruses and that bypassing this barrier allows several lineage B viruses to enter human cells through an unknown receptor. We also demonstrate how different lineage B viruses can recombine to gain entry into human cells, and confirm that human ACE2 is the receptor for the recently emerging SARS-CoV-2.
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              Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections

              The clinical features and immune responses of asymptomatic individuals infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have not been well described. We studied 37 asymptomatic individuals in the Wanzhou District who were diagnosed with RT-PCR-confirmed SARS-CoV-2 infections but without any relevant clinical symptoms in the preceding 14 d and during hospitalization. Asymptomatic individuals were admitted to the government-designated Wanzhou People's Hospital for centralized isolation in accordance with policy1. The median duration of viral shedding in the asymptomatic group was 19 d (interquartile range (IQR), 15-26 d). The asymptomatic group had a significantly longer duration of viral shedding than the symptomatic group (log-rank P = 0.028). The virus-specific IgG levels in the asymptomatic group (median S/CO, 3.4; IQR, 1.6-10.7) were significantly lower (P = 0.005) relative to the symptomatic group (median S/CO, 20.5; IQR, 5.8-38.2) in the acute phase. Of asymptomatic individuals, 93.3% (28/30) and 81.1% (30/37) had reduction in IgG and neutralizing antibody levels, respectively, during the early convalescent phase, as compared to 96.8% (30/31) and 62.2% (23/37) of symptomatic patients. Forty percent of asymptomatic individuals became seronegative and 12.9% of the symptomatic group became negative for IgG in the early convalescent phase. In addition, asymptomatic individuals exhibited lower levels of 18 pro- and anti-inflammatory cytokines. These data suggest that asymptomatic individuals had a weaker immune response to SARS-CoV-2 infection. The reduction in IgG and neutralizing antibody levels in the early convalescent phase might have implications for immunity strategy and serological surveys.
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                Author and article information

                Journal
                Science
                Science
                SCIENCE
                science
                Science (New York, N.y.)
                American Association for the Advancement of Science
                0036-8075
                1095-9203
                04 December 2020
                28 October 2020
                : 370
                : 6521
                : 1227-1230
                Affiliations
                [1 ]Department of General Internal Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
                [2 ]Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
                [3 ]Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
                [4 ]Clinical Microbiology Laboratory, Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
                [5 ]Division of Infectious Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
                [6 ]Department of Anesthesiology, Perioperative and Pain Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
                Author notes
                Author information
                https://orcid.org/0000-0001-5063-7016
                https://orcid.org/0000-0002-8029-8227
                https://orcid.org/0000-0003-1948-3834
                https://orcid.org/0000-0003-2628-9474
                https://orcid.org/0000-0002-7450-6624
                https://orcid.org/0000-0002-6754-7209
                https://orcid.org/0000-0001-6217-272X
                https://orcid.org/0000-0001-6792-7650
                https://orcid.org/0000-0002-6416-5096
                https://orcid.org/0000-0001-8162-0284
                https://orcid.org/0000-0003-0095-515X
                https://orcid.org/0000-0003-4121-776X
                https://orcid.org/0000-0003-0858-5624
                Article
                abd7728
                10.1126/science.abd7728
                7810037
                33115920
                64827fee-bc5c-400e-9108-df0475b417e5
                Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works

                This is an open-access article distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 10 July 2020
                : 26 October 2020
                Funding
                Funded by: doi http://dx.doi.org/10.13039/100000060, National Institute of Allergy and Infectious Diseases;
                Award ID: HHSN272201400008C
                Funded by: doi http://dx.doi.org/10.13039/100000060, National Institute of Allergy and Infectious Diseases;
                Award ID: 75N93019C00051
                Funded by: doi http://dx.doi.org/10.13039/100007457, JPB Foundation;
                Funded by: doi http://dx.doi.org/10.13039/100014895, Open Philanthropy Project;
                Award ID: #2020-215611
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                Seth Scanlon
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