A group of scientists have identified a gene that can inactivate HIV-1. These findings suggest a promising new strategy to combat the virus that causes AIDS.
In two of their studies, the scientists found that the host cell membrane protein called SERINC5 and SERINC3 greatly reduces the virulence of HIV-1 by blocking the ability of the virus to infect new cells.
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| HIV-1 virion. (Picture from: http://bit.ly/1WVOQZG) |
Disrupting this mechanism can be a powerful strategy for treating HIV and similar viruses that express the Nef protein.
Both of these studies use very different methodologies, but complementary. Both reveal a complex interaction between the HIV-1 Nef protein and cell surface membrane proteins SERINC5 and SERINC3, which are both expressed in T cells of the immune system.
Scientists show parallel sequencing on 31 different human cell lines in terms of large dependence on Nef for the replication of HIV-1.
They also approached the problem of biochemistry. By doing proteomic analysis of purified virions, they were able to identify host cell proteins are regulated by Nef.
"It has been known for more than 20 years that Nef is needed to make HIV-1, the deadly virus. Our new study may ultimately give us an important glimpse of how Nef might do this," said Prof. Luban.
HIV-1 consists of nine genes. To replicate the genome, the virus needs a host cell. Once the virus infects a cell, it will take over certain cellular processes so that it can replicate itself.
Ultimately, the infected host cells to produce new virions which carry the HIV-1 genome. These virions will then search for new cells to infect, continuing the cycle of infection.
Nef, one of the nine major HIV protein, induces a number of changes in host cells that enhance the ability of the virus to infect new cells.
One task is to absorb SERINC3 Nef and SERINC 5, so that the cellular protein can not reach the cell surface and can not join the newly formed virions.
One task is to absorb SERINC3 Nef and SERINC 5, so that the cellular protein can not reach the cell surface and can not join the newly formed virions.
In the absence of Nef, virions will join SERINC3 and SERINC5 protein into the viral sheath when they leave the host cells, making them unable to infect a new cell targets.
"These virions can attach itself to a target host cells, but the genome of HIV-1 can not pass through the veil of viral when there SERINC3 and SERINC5. Somehow, this protein can inhibit the release of the viral genome, which essentially prevent the spread of the virus, "explains Prof. Gottlinger.
Scientists say that the effect of anti-retroviral from SERINC seems to reach all retroviruses and may turn into a universal. *** [EKA | FROM VARIOUS SOURCES | SCI-NEWS.COM]
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