The mechanism by which SARS-CoV-2 virus disrupts protein synthesis in infected cells and thus acts against the immune system has been studied.
German scientists from the University of Munich and the University of Ulm Hospital have published an article in the journal Science about the causes of the dangerous features of the infection.
It was found that the main role in the pathogenic mechanism is played by the viral protein Nsp1. It helps the SARS-CoV-2 virus to capture and multiply in cells: Nsp1 interacts with the 40S ribosomal subunit, which binds mRNA to ribosomes and ensures subsequent protein synthesis, thereby preventing it from binding to mRNA. takes. Thus, protein synthesis stops. This causes one of the body's main defense systems against infection to fail.
The innate immune response no longer responds because a significant signal cascade stops working due to Nsp1. Impaired primary immunity leads to the development of other fatal symptoms in patients, including "cytokine storms".
Scientists believe that one of the possible approaches to neutralize the coronavirus may be to develop a drug that prevents Nsp1 from binding to the ribosomal subunit.