a common virus called human herpesvirus 6 (hhv-6) prevents a form of the aids virus from reproducing. This was found during a laboratory study on cultures of human tissue. The study team led by Leonid Margolis of the us -based National Institute of Child Health and Human Development (nichd), included researchers from the San Raffaele Scientific Institute in Milan, Italy. The team found that hhv-6 hinders the growth of hiv variants that transmit infection at the early stages of the disease's manifestation. However, it is not able to do so during later stages of the disease.
Both the early and late stage variants of hiv bind to target cells by means of a 'receptor complex'. Molecules on the surface of hiv bind to molecules on the surface of immune cells. Then the hiv virus fuses with the cell and infects it. The process usually involves hiv binding to a receptor known as cd 4 . However, in order to fuse with a cell, hiv also needs to bind to another receptor on the cell's surface. hiv-1 variants that transmit infection and dominate the early stages of the infection bind to a molecule known as ccr 5 . As the disease progresses, these viruses are often replaced with other variants, which bind to another receptor called cxcr 4 .
Margolis and his colleagues infected human tonsil tissue with hiv and hhv-6 . Tonsils are part of the lymphoid system, the network of immune cells and molecules that regulate the body in search of disease causing organisms. They found that the hiv variants that use ccr 5 do not reproduce as fast in tissue blocks that are also infected with hhv-6 as they do when contained in tissues that are free of hhv-6 . However, the hiv-1 variants that use cxcr 4 and are typical for the late stages of disease reproduce slightly more rapidly in cultures containing hhv-6 . These variants typically kill more immune cells than do the ccr 5 variants.
The researchers also discovered the molecular mechanism by which hhv-6 affects hiv-1 reproduction. Tissues infected with hhv-6 produced large amounts of a molecule called rantes, which apparently blocks the ccr 5 receptor. Therefore, by triggering rantes production, hhv-6 deprives the early hiv variant of its binding site, which, in turn, prevents the hiv virus from entering the cell. as added proof of this mechanism, the researchers added rantes to cultures containing only the ccr 5 -using hiv variant. As expected, the reproduction of these viruses was suppressed.
Margolis says that their research could have significant implications for future aids treatment. Duane Alexander, director of the nichd, agrees with him. "Future research on hhv-6 could lead to new drugs that can better help the immune system to fend off hiv and may even lead to new strategies for making aids vaccines," said Alexander.
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