Us vs. HIV

During the opening era of the AIDS epidemic, being diagnosed was a death sentence. Thanks to advances in medicine, it isn't anymore. HIV is no longer a terminal illness; with treatment, an individual with HIV has the exact same life expectancy as someone without the disease.

However, it is still a devastating virus. The treatments have many side effects, and you will need to take the medicine for the rest of your life.

For years, scientists have been trying to find a way to effectively cure HIV/AIDS, but unfortunately, none yet have made that incredible leap. But new breakthroughs come each year, which slowly bring us closer to our goal.

Case in point, last month, researchers from the University of Massachusetts Medical School announced the discovery of proteins that naturally inhibit the human immunodeficiency virus. Surprisingly, they found these proteins in the cells in our immune system’s T cells, which are the cells that HIV attacks (specifically, it attacks CD4 positive T cells, which are white blood cells that are vital to fighting off infection).

To break this down a bit, the researchers found that host cell membrane proteins, called SERINC5 and SERINC3, reduce the virulence of HIV-1 by more than 100-fold. Ultimately, they do so by blocking the ability of the virus to infect new cells.

However, HIV also has a trick up its sleeve.

The HIV-1 Nef, a protein important for the development of AIDS, counteracts the SERINCs. The researchers believe that drugs that could target Nef would permit the SERINC proteins to inactivate the virus. Disrupting this mechanism could be a strategy for treating HIV and similar viruses that express the Nef protein

SERINCs and Nef

HIV-1 only has nine genes in its genome that can only be replicated with a host cell. Once infected, the host cell produces new virions carrying the HIV-1 genome. These virions, in turn, search for new cells to infect, continuing the cycle of infection.

Nef, is one of nine primary HIV proteins that increases the virus’s ability to infect new cells. It sequesters SERINC3 and SERINC5 so that these cellular proteins do not reach the surface of the cell and cannot be incorporated into newly formed virions. Thus, with Nef out of the picture, virions incorporate the SERINC3 and SERINC5 proteins into the viral envelope as they leave the host cell, rendering them unable to infect new target cells.

These results were published in the journal Nature.


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