
WEBINAR
Only
Preparing for Emerging Viral Diseases: Lessons from SARS-CoV-2
Wednesday, September 30, 2020, 10:30 AM - 5:30 PM EDT
WEBINAR
Presented By
The New York Academy of Sciences
The current COVID-19 pandemic has brought the risks of emerging viral pathogens into sharp relief. Eight months into the pandemic, more than 18 million cases have been confirmed, and at least 700,000 people have died worldwide. Moreover the economic ramifications of prolonged shut downs are severe and likely to persist long term. However, the scientific community has mobilized like never before and rapid advances are being made in therapeutic and vaccine development. Technologies developed to combat other recent epidemics such as SARS and Ebola are now being adapted to fight SARS-CoV-2, underlining the importance of developing scientific tools that can quickly be modified and deployed against new viral threats. This symposium will examine state-of-the-art methodologies for pathogen surveillance and identification, viral characterization, and therapeutic and vaccine development. While the symposium will focus on the latest research on SARS-CoV-2, the broader goal is to highlight best practices for preparedness against future viral threats.
The Panel Discussion for this program is organized by Junjun Gao, PhD, Boehringer Ingelheim and Neil Stahl, PhD, Regeneron.
Registration
Wednesday
September 30, 2020
Introduction and Welcome Remarks
Keynote: Preparing for the Next Pandemic
Speaker
Session 1: Surveillance and Pathogen Identification
Emerging Pathogens: Origins and Identification
Speaker
From the first documented pandemic almost 2,000 year ago to our new reality in this time that will forever be marked by COVID-19, infectious diseases, caused by pathogens that have evolved in animals, have plagued humanity, resulting in huge tolls that can be measured in lives lost, economic impacts, and social instability. There are an estimated one billion cases of zoonotic diseases in people annually, and numerous other species are threatened or on the brink of collapse from a combination of anthropogenic pressures, including human-driven infectious disease transmission. Epidemics due to emerging viral diseases, in particular those caused by viruses with origins in wildlife hosts, are increasing in both frequency and severity. Spillover of these viruses from wildlife can be directly attributed to human activities. Human-induced landscape change, especially deforestation, intensification of agricultural production, and urbanization associated with human population growth, has disturbed ecological balances, altered transmission dynamics in all hosts, increased contact between people and animals, and driven virus spillover and the amplification and spread of pathogens. After a decade of employing a One Health approach to viral detection, discovery, and characterization, we can reasonably estimate that there are more than 500,000 zoonotic viruses that have the potential to spillover from evolutionary host species to vulnerable ones, including humans. We know how to approach identifying nearly all of the viral diversity in every species and can begin to rank the risks of these viruses for interspecies transmission. Understanding the disease threats and developing mitigation strategies to prevent infection and spread of viruses are key to preventing future devastating pandemics.
Break
Session 2: SARS-CoV-2: Molecular Virology, Models and Host Immunity
Coronaviruses: Old and New
Speaker
Coronaviruses: Old and New
Part I: Introduction and history coronaviruses dating back to the 1980s and coronavirus biology. I will describe the coronavirus life cycle pointing steps that may serve as targets of antiviral therapies that may effective against most if not all coronaviruses.
Part II. Coronaviruses are highly effective in antagonizing host innate immune responses, more specifically interferon (IFN) induction and signaling pathways. MERS-CoV and SARS-CoV fail to induce IFN early in infections of humans and in mouse models while IFN production in late disease may be pathogenic. Antagonism of host responses is carried out through expression of multiple viral accessory proteins as well as conserved replicase encoded proteins, sometimes with redundant activities. Our lab focuses on the double-stranded RNA induced antiviral pathways: type I and types III IFNs, oligoadenylate synthetase-ribonuclease (OAS-RNase L) and protein kinase R (PKR). Activation of these pathways leads to inhibition of viral replication, shut down of protein synthesis and apoptotic cell death. I will discuss coronavirus antagonism of these pathways using examples from our previous studies of the betacoronaviruses murine coronavirus MHV and MERS-CoV and recent data on SARS-CoV-2. Our findings suggest that sARS-coV-2 less adept at antagonizing dsRNA induced pathways than MERS-CoV and MHV.
Learning Objectives
Coronaviruses enter cells by two pathways, at the plasma membrane fusion or through endosomes
Coronaviruses encode 16 conserved non-structural proteins in the replicase locus, potential targets for pan coronavirus antivirals
Coronaviruses are adept at antagonizing activation of dsRNA induced antiviral pathways, including interferon signaling, OAS-RNase L and PKR.
Virology of SARS-CoV-2
Speaker
Break
Using Systems Serology to Define Correlates of Immunity to SARS-CoV-2
Speaker
Session 3: Therapeutic Interventions and Vaccines for SARS-Cov2 and Beyond
The Expedited Development of an Antiviral Agent for the Treatment of SARS-CoV-2 Infection
Speaker
Neutralizing Antibodies and other Therapeutic Approaches
Speaker
COVID-19: A Prototype Pathogen Demonstration Project for Pandemic Preparedness
Speaker
Break
Session 4: Panel Discussion
Perspectives on Therapeutics and Vaccines for COVID-19
Speakers