![]() ![]() Nonstructural proteins nsp7 through nsp16 form the core of the RTC and represent a prime target for antiviral drug development, as the function of the core replicase is highly conserved. A multiprotein complex formed by coronaviruses termed the replication transcription complex (RTC) is responsible for RNA replication and proofreading. In general, any inactivation of these proteases leads to a loss of RNA synthesis, and it is well established that viral RNA replication and viral protease functions are vulnerable to intervention. DR.CHRISTOPHER REEDER PROWithin the polyprotein are 2 proteases, the papain-like protease (PL pro) and 3CL pro (also known as nsp5 or M pro, short for main protease). Two-thirds of the SARS-CoV-2 genome is dedicated to the synthesis of 2 replicase polyproteins called polyprotein 1a and polyprotein 1ab. Cellular entry of coronaviruses, such as SARS-CoV-2, occurs primarily via the spike (S) proteins of SARS-CoV-2 binding to the host ACE2 (angiotensin-converting enzyme 2) receptor. OVERVIEW OF THE VIRUS AND THERAPEUTICS APPROACHESĬoronaviruses are enveloped positive-sense single-stranded RNA viruses enclosed by capsid comprised of multiple proteins, most notably the spike proteins that are responsible for the virus’s crown-like appearance. The meeting agenda is shown ( Box 1), and the principal session topics were: DR.CHRISTOPHER REEDER UPDATEAn update on vaccines and neutralizing antibodies was provided, and a final summary session was held to identify key points from the Summit. In each panel, the session moderator provided an overview of the topic (slides are included in the Supplementary Material) and facilitated discussion with panelists. The Summit itself comprised introductory remarks, an overview of SARS-CoV-2 replication and therapeutic targets, and 5 scientific panels that followed. ![]() The meeting moderators and panelists were from academia, industry (pharma/biotech), NIH Institutes and Centers, and Federal agencies working in the COVID-19 therapeutics space. The Summit was jointly organized by National Institute of Allergy and Infectious Diseases (NIAID), National Center for Advancing Translational Sciences (NCATS), and the National Institutes of Health (NIH) Office of the Director, and hosted by Dr Francis Collins (NIH), Dr Anthony Fauci (NIAID), and Dr Christopher Austin (NCATS). The goals of the Summit were to review the current state of the science, identify unmet research needs, share insights and lessons learned from treating other infectious diseases, identify opportunities for public-private partnerships, and assist the research community in designing and developing antiviral therapeutics. Scientific experts from the public and private sectors convened to discuss severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) targets for drug discovery, and the preclinical tools needed to develop and evaluate effective small-molecule antivirals. The Virtual Summit was organized to provide an overview on the status and challenges in developing antiviral therapeutics for coronavirus disease 2019 (COVID-19), including combinations of antivirals, and it was streamed live to allow broad public access while maintaining social distancing. The NIH Virtual SARS-CoV-2 Antiviral Summit was held on 6 November 2020. INTRODUCTION TO THE NIH VIRTUAL SARS-COV-2 ANTIVIRAL SUMMIT ![]() This report includes an overview of therapeutic approaches, individual panel summaries, and a summary of the discussions and perspectives on the challenges ahead for antiviral development. Scientific experts from the public and private sectors convened virtually during a live videocast to discuss severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) targets for drug discovery as well as the preclinical tools needed to develop and evaluate effective small-molecule antivirals. The NIH Virtual SARS-CoV-2 Antiviral Summit, held on 6 November 2020, was organized to provide an overview on the status and challenges in developing antiviral therapeutics for coronavirus disease 2019 (COVID-19), including combinations of antivirals. ![]()
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