Scientist’s have recently identified two genes that possibly could slow down and potentially stop HIV-1 ability to infect new cells. These genes could potentially lead to new strategies of battling the virus, HIV-1, that leads to AIDS.

HIV-1 virion. Image credit: US National Institute of Health.

In two studies, they discovered that the proteins, SERINC5 and SERINC3, which cover the cell membrane of host’s cells; can greatly disrupt the the HIV-1 ability to infect new cells and overtake the bodies autoimmune system.  By impeding this virulence, it can greatly reduce the number of cells taken over by the virus and thus delay AIDS from happening. HIV-1 infects cells by having a protein, called HIV-1 Nef, by inhibiting the host immunologic response to HIV inhibiting death of infected cells by apoptosis (cell suicide by bursting). It counteracts the SERINCs. This allows the HIV-1 virus to promote its own replication and slowly destroy the bodies auto-immune system.

Prof. Jeremy Luban. from U MA Medical School, comments “It’s amazing, the magnitude of the effect that these proteins have on infectivity. The SERINC proteins reduce the infectivity of HIV-1 virions by more than 100-fold,” New drugs that target this Nef protein could permit the bodies natural defenses, the SERINCs, to incapacitate the virus and possibly stop HIV-1 from spreading and transitioning to AIDS.

In two separate studies, both used different ways to show the relationship between the HIV-1 Nef and the SERINCs, both of which are apart of the immune system’s T cells. The researchers used parallel sequencing on 31 human cell lines. Each cell line differed in their reliance on Nef for HIV-1 replication. They also conducted proteomic analysis to identify the proteins that Nef regulated.

They found that Nef shuts down the SERINC3 and SERINC5 proteins so that they can not be incorporated in the newly formed virons. When there is no Nef the virons replicate with SERINC3 and SERINC5 proteins into their viral envelope. This renders them unable to infect new cells by not letting the virus pass through other uninfected cells. Prof. Gottlinger, also from U MA Medical School, states, “Somehow these proteins are blocking the release of the virus’s genome, essentially keeping the virus from spreading.”

Using this information we can create new medicines that inhibit the Nef protein and slow down the spreading of HIV-1. This is a major breakthrough in AIDS treatment and could vastly improve the longevity of AIDS patients.

HIV Life Cycle