04 March 2008

You can fight HIV from the inside

Canadian scientists from the University of Alberta, working under the guidance of Dr. Stephen Barr, in experiments on cell culture, found that the introduction of the TRIM22 gene into cells infected with the human immunodeficiency virus blocks the assembly of HIV particles and thus prevents infection of other cells.

Proteins of the interferon family are synthesized by cells in response to the penetration of pathogens into the body, including viruses. Type 1 interferons (-alpha and -beta) are synthesized by many types of cells, and type 2 interferon (-gamma) is synthesized by immune cells. When human cells infected with HIV are introduced into the culture, type 1 interferons suppress the replication of the virus, but the molecular mechanisms of this process have so far been completely unclear.

In earlier studies, scientists found that exposure to type 1 interferons significantly increases the expression of the TRIM22 gene. In addition, the relationship between the activity of this gene and the suppression of HIV reproduction in cell cultures was revealed. By selectively blocking the activity of the TRIM22 RNA interference gene, the authors demonstrated that this gene is a key mediator of the interferon-beta-mediated antiviral immune response. They found that the protein product of the TRIM22 gene blocks the intracellular movement of the structural viral protein Gag to the cell surface.

This means that the TRIM22 gene is an important factor ensuring the resistance of our body to HIV, and the results indicate that there is a gene in the human genome that can stop the spread of HIV infection.

One of the main problems in the fight against HIV is the ability of the virus to mutate and acquire resistance to drugs. Anti-retroviral drugs that appeared in the late 1990s suppress the ability of the virus to reproduce, however, despite their effectiveness, they do not allow the virus to be completely removed from the body. The gene discovered by the authors may allow solving this problem in a natural way.

Currently, the authors are searching for reasons why the molecular mechanism acting "in vitro" does not work in vivo – in people infected with HIV. Having found out these reasons, it will be possible to try to find a way to activate the TRIM22 gene in the body of HIV-infected patients. Scientists hope that the results of their work will lead to the emergence of new drugs that suppress the transmission of the virus from person to person and its spread through the body, thus preventing the development of AIDS.

Another task that the researchers have set themselves is to find out the ability of the TRIM22 gene to prevent the spread of other viruses.

Article by Stephen D. Barr et al. "The Interferon Response Inhibits HIV Particle Production by Induction of TRIM22" is published in PLOS Pathogens.

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04.03.2008

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