Thread by @vipintukur

COVID’s – and other viruses’ – Achilles' heel identified!

Researchers have identified how the SARS-CoV-2 virus that causes COVID-19 takes advantage of our cellular machinery to replicate and spread in the body, and, importantly, a way to stop it. 1/

The finding could lead to the development of a new class of antiviral therapies to treat not only SARS-CoV-2, but other viruses as well. 2/

Genetic instructions in our cells are transcribed from DNA to mRNA, then translated into proteins that enable functions such as cell-to-cell communication. 3/

After translation, these proteins need additional modifications, called post-translational modifications, to ensure they perform effectively. 4/

SUMOylation* is one such post-translational modification that directly regulates viral replication and the body’s innate immune response.

*Small Ubiquitin-like modifier (SUMO) 5/

Researchers in a new study examined the post-translational modification mechanism that occurs during infection with SARS-CoV-2 to see if there is a way to stop its spread. 6/

mdpi.com/1999-4915/15/7…

A core component of the SARS-CoV-2 virus is the nucleocapsid (N) protein, mainly responsible for packaging RNA in a protective covering. SUMOylation directs the virus’ N protein to the right location for packaging after it infects human cells. 7/

Once it’s in the right place, the protein begins inserting copies of its genes into new infectious virus particles, virions, which spread and make us sicker. In the wrong location, the virus cannot infect us. 8/

If someone gets an infection, maybe one of his or her proteins will appear differently than it was before. 9/

In this study, researchers identified three SUMOylation sites on the SARS-CoV-2 N protein. One of the sites, K65, was critical to the protein’s nuclear translocation, or the movement of proteins into the cell’s nucleus, a novel feature of the SARS-CoV-2 virus. 10/

The researchers concluded that the spread of the virus depends on SUMOylation proteins and that blocking access to the proteins would enable our immune system to kill it.

A new medication based on this discovery would be useful to patients in all stages of infection. 11/

The researchers say identifying the similarity of action between SARS-Cov-2 and the influenza virus may lead to the development of a new class of antiviral medications with broad application. 12/

They conclude that other viruses might work this way as well. Ultimately, we would like to block the flu as well as COVID, and potentially other viruses such as RSV and Ebola. 13/

newatlas.com/medical/achill…