COVID-19 can lead to severe symptoms and rapidly fatal, it attacks a patient's acute immune system and weakens them.
For now, researchers are focused on figuring out how the virus attacks the immune system to devise interventions.
A new study published May 12, 2021 in the journal Nature has revealed a way viruses use to maintain rapid division and replication in a patient's body, without being attacked by the immune system. detect.

The research team, including Dr Noam Stern-Ginossar from the Weizmann Institute of Science and Dr Nir Paran, Dr Tomer Israely from the Israel Institute of Biological, Chemical and Environmental Sciences, focused on understanding how whose molecules are active in cells infected with SARS-CoV-2.

In normal cells, when infected, they quickly send out an invasion warning signal. These signals notify the immune system of a virus "attack". But, with SARS-CoV-2, the cells do not seem to detect the attack of the viral groups leading to a delayed immune response, which has facilitated the virus to rapidly replicate and multiply. flourish without hindrance.

By the time the immune system responds… usually it is too late, the condition has become serious and harmful to the host and causes impairment of the entire body.

Stern-Ginossar said: "Most current research is focusing on viral proteins (the protein coat of a virus) to determine their function. However, so far there is no precise information about these what's going on in the infected cells themselves, so we tested infecting healthy cells with the virus and assessed how the infection affects important biochemical processes important in the cell such as gene expression and protein synthesis".

When cells are infected with a virus, they begin to develop a series of antiviral genes - genes that are like the cell's front-line defenders, sending out warning signals to neighboring cells. to activate the immune system against viral infections.

At this point, both the cell and the virus "race" for the ribosomes, the protein-synthesizing "factories" for the cell, where the virus itself is also in short supply. After that, of course, there was a real "war" between "our side" and the virus to protect this precious resource.

The study sheds light on how SARS-CoV-2 gains the upper hand in battle, specifically: within hours, the virus rapidly takes over the protein-making machinery of the cell and deactivates the antiviral. inhibits foreign cell invasion, interrupts virus detection signals both internally and externally, and delays and disrupts the immune response.

The researchers have shown that the virus can attack a cell's hardware, taking over its protein synthesis machinery using three distinct, complementary tactics. The first tactic the virus uses is to reduce the cell's ability to synthesize proteins. The second tactic is to degrade cellular messenger RNAs (mRNAs) (molecules that carry protein production information from DNA to ribosomes).

Finally, the virus interferes with the production of mRNA from the cell nucleus to the main chamber of the cell, which serves as a template for protein synthesis. By using this three-way tactic, which is unique to SARS-CoV-2, the virus can effectively implement its ability to "shut down the host" to take over the host's ability to take over as well as synthesize proteins. cell.

In this way, important messages from the antiviral genes that cells produce during infection do not reach the factory to produce active proteins that lead to an immune response, Stern-Ginossar explains. delayed.

However, the good news is that this study succeeded in identifying the viral protein envelope involved in host shutdown by SARS-CoV-2, which may offer new opportunities in developing effective treatments for COVID-19.

Stern-Ginossar's research was funded by the Skirball Chair in New Scientists; Knell Family Center for Microbiology; American Commission on Experiments and Weizmann Institute of Science 70th Anniversary; Ben B. and Joyce E. Eisenberg Foundation; Bioresources Maurice and Vivienne Wohl.

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