Studies Reveal Potential Weaknesses In SARS-CoV-2 Infection
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A study published in the journal Cell online on December 8 revealed that TMEM41B also known as transmembrane protein 41 B was essential for SARS-CoV-2 to replicate, is believed to help shape the fatty outer membrane that protects the virus' genetic material while it replicates inside an infected cell and before it infects another.

Researchers compared how the COVID-19 virus reproduces in infected cells to the same processes in two dozen deadly flaviviruses, including those responsible for yellow fever, West Nile and Zika disease.

These studies represent the first evidence of transmembrane protein 41 B as a critical factor for infection by flaviviruses and, remarkably, for SARS-CoV-2. 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, said the researchers.

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, or pathways, involved in 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 mutation are less vulnerable to the disease. The research team next plans to map out TMEM41B's precise role in SARS-CoV2 replication so they can start testing treatment candidates that may block it.

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