According tomedia reports, getting rid of the new coronavirus infection is one of the priorities of doctors to treat patients with new coronary pneumonia. Some treatments are in the experimental stage, in which doctors try to use a variety of drugs to treat new coronary pneumonia and help the immune system kill the virus. But now scientists have begun to study how the virus is trying to moderate the immune system’s response, and they think they already know what drugs can kill the virus.
In a new study, Virologist Benjamin Ten Oever and his team explain how SARS-CoV-2 interferes with the immune response of some patients, while also describing how COVID-19 infections can cause potentially fatal cytokine storms.
“This is something I’ve never seen in 20 years of studying the virus, ” the researchers told Stat. It is understood that the new coronavirus is very cunning, it can block the cell “call to arm” the gene but can make the “call to strengthen” the gene continues to function. All viruses interfere with both genes, but SARS-CoV-2 only blocks genes that fight the virus soon after infection.
Ten Oever refers to the “call to arms” is the gene that produces interferon. When a cell is infected by a pathogen, the cells are released and neighboring cells are told to activate their own cells, slowing the replication of the virus. This process can last 7-10 days and can buy time for gene enhancement calls.
The second group of genes produced chemokines that sounded the alarm for the immune system’s B and T cells. B cells identify the virus and produce antibodies to it, which then play a role in the COVID-19 immune system, while T cells are responsible for removing the virus.
What happened next is not surprising. Viruses replicate at will, and millions of copies infect other cells. While all of these cells produce interferons that help reduce replication, viruses block this mechanism. At the same time, B and T cells are called together, which can lead to large-scale inflammatory reactions. This is the “unique” and “abnormal” result of how SARS-CoV-2 manipulates the target genome.
Ten Oever points out that without interferon, there is nothing to stop the virus from replicating and festering forever in the lungs, because his team found no trace of interferon in the lung cells of COVID-19 patients. However, the lungs will express more and more “enhanced signal” genes, which will lead to more and more immune cells.
That is, without interferon to stop the virus from replicating, the lung cells will be killed and the lung’s respiratory function will be affected. “All of a sudden you’re in the hospital, having trouble breathing,” ten Oever said.
The elderly and people with diabetes, heart disease and other diseases are all at risk of the disease. Even without the presence of pathogens, their interferon genes are much weaker than those of young people. This explains why they can also deal with new coronavirus infections and why they experience an increased inflammatory response.
In a separate non-peer-reviewed study, researchers from Japan noted that the new coronavirus has a gene called ORF3b, which exhibits strong anti-interferon activity. This will prevent cells from recognizing the presence of viruses and interferon genes from being activated.
Stat said the findings could lead to interferon-based treatments that counteract the virus’s effects on interferon genes. A third study, published in preprinted form by researchers at the University of Texas Medical Division, showed that interferon IFN-1 could effectively block the replication of new coronaviruses under laboratory conditions. Vineet Menachery and his team have also shown that if IFN-1 is added to a petri dish, the virus is difficult to replicate. After a few days, interferon-treated cells had a viral load 1,000 to 10,000 times lower than cells that the virus could replicate at will. Stat, however, points out that clinical trials are needed to determine the course of action.