As all viruses, SARS-CoV-2 is in the grey zone between a chemical and a living being. Its biological machinery is too scant to propagate on its own, and instead the virus hijacks proteins of the host to generate new copies of itself. Scientists hope that by developing drugs that disrupt such proteins, it might become possible to deal a fatal blow to the virus. Now a new study (titled “Genome-Scale Identification of SARS-Cov-2 and Pan-Coronavirus Host Factor Networks”) maps out this intricate network of helpers for SARS-CoV-2 and three other coronaviruses that cause the common cold. The results identify over a hundred human proteins without which these viruses cannot replicate inside the cells and cause disease.Among them is a protein that stands out because it is an absolute requirement for infection by the four coronaviruses. Moreover, it is also needed by viruses from an entirely different family, flaviviruses, including those that cause yellow fever, West Nile, and Zika disease, according to results of a second study (titled “TMEM41B Is a Pan-Flavivirus Host Factor”). “The fact that this protein is important to multiple different viruses makes it a promising and high-priority target for drug development efforts,” says Charles M. Rice, PhD, Professor of Virology at Rockefeller University, who co-led the studies with John Poirier, PhD, Assistant Professor, Medicine, at New York University. Both studies were published in Cell. The TMEM41B article was published online on December 8, 2020, and the Genome-Scale Identification article was published online on December 9, 2020. Once it has entered a host cell, SARS-CoV-2 co-opts hundreds of molecules to make copies of the viral RNA and wrap them up as thousands of new viruses.
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