Potential Weaknesses in SARS-CoV-2 Infection Discovered

Transmembrane protein TMEM41B was essential for SARS-CoV-2 to replicate, said researchers.

Transmembrane protein 41 B (TMEM41B) necessary for the coronavirus to reproduce and spread to other cells was a potential weakness that could be targeted by future therapies, revealed a study published in the journal Cell.

The //transmembrane protein helps shape the fatty outer membrane that protects the COVID-19 virus' genetic material while it replicates inside an infected cell and before it infects another.

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‘CRISPR that maps the molecular weaknesses in SARS-CoV-2 serves as a model for scientists worldwide for confronting future viral outbreaks.’

The latest finding comes from a pair of studies led by researchers at NYU Grossman School of Medicine and NYU Langone Health's Perlmutter Cancer Center, and colleagues at Rockefeller University and elsewhere.

Researchers compared how the COVID-19 virus reproduces in infected cells in deadly flaviviruses, including those responsible for yellow fever, West Nile, and Zika disease. They also compared how the virus replicates in infected cells to three other seasonal coronaviruses known to cause the common cold.

"Together, our studies represent the first evidence of transmembrane protein 41 B as a critical factor for infection by flaviviruses and, remarkably, for coronaviruses, such as SARS-CoV-2, as well," says the studies' co-senior investigator John T. Poirier, PhD.

Coronavirus
Coronaviruses infect animals, humans, and birds. Human coronaviruses, such as SARS, MERS, and 2019-nCoV cause respiratory distress and even death. The S protein is the infectious agent of the virus.

"An important first step in confronting a new contagion like COVID-19 is to map the molecular landscape to see what possible targets you have to fight it," says Poirier, an assistant professor of medicine at NYU Langone Health.

"Comparing a newly discovered virus to other known viruses can reveal shared liabilities, which we hope serve as a catalogue of potential vulnerabilities for future outbreaks."

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"While inhibiting transmembrane protein 41 B is currently a top contender for future therapies to stop coronavirus infection, our results identified over a hundred other proteins that could also be investigated as potential drug targets," says Poirier, who also serves as director of the Preclinical Therapeutics Program at NYU Langone and Perlmutter Cancer Center.

CRISPR, the gene-editing tool, was used to inactivate each of more than 19,000 genes in human cells infected with each virus, including SARS-CoV-2. Researchers then compared the molecular effects of each shutdown on the virus' ability to replicate.

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In addition to TMEM41B, some 127 other molecular features were found to be shared among SARS-CoV-2 and other coronaviruses. These included common biological reactions, pathways, cell growth, cell-to-cell communication, and means by which cells bind to other cells.

More research is needed to determine if TMEM41B mutations directly confer protection against COVID-19, and if East Asians with the mutations are less vulnerable to coronavirus pandemic.

Source-Medindia