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A promiscuous interaction of SARS-CoV-2 with bacterial products
Guillaume Carissimo1,2 , Lisa F.P. Ng1,2,3,*
1A*STAR Infectious Disease laboratories (A*ID Labs), Agency for Science, Technology and Research, Immunos, Singapore 138648, Singapore
2Singapore Immunology Network (SIgN), Agency for Science, Technology and Research, Immunos, Singapore 138648, Singapore
3Institute of Infection, Veterinary and Ecological Sciences, University of Liverpool, Liverpool L7 3EA, UK
*Correspondence to:Lisa F.P. Ng , Email:lisa_ng@immunol.a-star.edu.sg
J Mol Cell Biol, Volume 12, Issue 12, December 2020, 914-915,  https://doi.org/10.1093/jmcb/mjaa068

SARS-CoV-2 is the virus responsible for COVID-19 disease, and since its emergence it has spread globally with the number of total cases in the tens of millions. COVID-19 presents with varied clinical manifestations that range from asymptomatic disease to severe respiratory disease (pneumonia) with multiple organ failure and death. Several risk factors have been associated with severe COVID-19 disease such as age, gender, diabetes, cardiovascular disease, treatments, and comorbidities that affect the immune system (Harrison et al., 2020). As is often the case for pathogen infections, the host immune system is a key player in virus clearance and resolution of disease. Nevertheless, a wealth of evidence has emerged to implicate the host’s immune system in the outcome of disease severity. In this case, an imbalance between inflammation and protection leads to the progression to more severe disease.