Methods to treat HIV (Human Immunodeficiency Virus) have improved greatly since the virus first began to affect humans, in the late 1980s. A few of those infected never developed full-blown AIDS, but for the majority, the inevitable result would have been wasting away due to an inability to fight diseases. Treatment for HIV has improved continuously, and the disease is no longer considered to be fatal once the affected person receives treatment. These treatments have at least two disadvantages, however: they would need to be continued for the duration of the individual’s lifetime and there are also uncomfortable side effects. Researchers are confident that there will eventually be a cure for HIV, and they continue to do tests that may take us closer to finding one.
Scientists from The University of Massachusetts Medical School have published an article in Nature, which states the possibility of decreasing the spread of HIV using cells which occur naturally in our bodies. Ironically, these are the same cells which the virus attacks. HIV breaks down the immune system by infecting and destroying CD4 positive ‘helper’ T-cells.
These white blood cells are vital to fighting off infection, which is why HIV is so efficient at wrecking havoc in the immune system. After affecting some of the cells, the virus uses these to travel through the body and infect other CD4s. T-cells transport these by settling in between lymph nodes, and others areas, that the free virus would be unable to reach.
The researchers found that there are proteins in the T-cells in our immune system which naturally fight HIV. SERINC5 and SERINC3, two host cell proteins, are able to stifle HIV-1 by greater than 100-fold. The HIV-1 genome has nine genes which can be replicated in the host cell, which then produce virions (the infectious part of the virus). They begin a cycle of infection by looking for new cells to infect. One of these, NEF (which is a key part in the development of AIDS) helps the process by blocking the SERINC proteins, so that they are unable to reach the cell’s surface. This means that they will no longer become a part of the newly formed virions. Developing a drug to restrict NEFs would allow the system to fight HIV, as the virions would then include SERINC3 and SERINC5 making them unable to infect new cells. This process could then be applied to other infectious viruses with NEF proteins.