Professor Edward Stevens and his colleagues drew attention to the fact that a new type of coronavirus and HIV use approximately the same mechanisms for the formation of pores in the shell of infected cells.
Molecular biologists have found out that one of the proteins of the SARS-CoV-2 envelope blocks the work of cellular systems that are critical for the penetration of HIV into cells and the formation of new particles of the immunodeficiency virus. The results of the scientists’ experiments were published in an article in the electronic library bioRxiv.
“Our experiments have shown that the coronavirus protein E, which is critical for the “escape” of viral particles from infected cells, prevents the immunodeficiency virus from successfully infecting human cells. This is due to the fact that this viral peptide interferes with the assembly of HIV proteins and causes cells to destroy them more often,” the researchers write.
In recent years, scientists have conducted several dozen studies on how often people are simultaneously infected with various viral infections. A group of American molecular biologists led by Edward Stevens, a professor at the University of Kansas in Kansas City (USA), has discovered another unusual example of the interaction of viruses simultaneously present in the human body.
Professor Stevens and his colleagues drew attention to the fact that a new type of coronavirus and HIV use approximately the same mechanisms for the formation of pores in the shell of infected cells, through which new viral particles leave them. This forced scientists to compare the structure and mechanisms of the shell proteins E and Vpu, which SARS-CoV-2 and HIV use to form holes in the cell envelope.
During this comparison, the researchers tested what would happen if one of these proteins was injected into the culture of infected or healthy cells, and then they tried to infect them with the immunodeficiency virus or SARS-CoV-2. These experiments showed that infected cells almost stopped producing new HIV particles if biologists pretreated them with a solution of protein E.
Biologists obtained similar, though less pronounced results during experiments with protein E analogues produced by SARS-CoV-1 and HCoV-OC43 viruses, pathogens of atypical pneumonia and colds. Such a discovery forced Professor Stevens and his colleagues to study in detail how the appearance of protein E inside cells affects the production of new HIV particles.
Subsequent experiments indicated that the coronavirus proteins did not interfere with the integration and reading of the HIV genome, but at the same time they suppressed the production of its proteins necessary for the assembly of new viral particles or playing an important role in infecting cells. In addition, the scientists found that protein E activated cellular systems that promote the purification of infected cells from viral proteins.
According to Professor Stevens and his colleagues, scientists cannot yet say why this is happening, as well as how coronaviruses acquired such an ability. Subsequent experiments, the researchers hope, will reveal the history of the evolution of protein E and allow scientists to understand whether it will be possible to adapt it to fight HIV.