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Your support makes all the difference.A NEW approach to Aids therapy which uses the body's own immune system to keep the HIV virus 'locked up' in infected cells is being developed.
Researchers in California have identified a cell in the immune system which stops replication of the virus, it was revealed at the conference yesterday. It attacks infected cells and kills the virus.
The onset of symptoms in HIV and Aids is marked by a drop in the activity of this cell, known as CD8, according to Jay Levy, Professor of medicine at University College San Francisco. He and his team have shown that CD8 activity is strong in HIV positive people who remain healthy.
It appears that the CD8 mechanism is also responsible for reducing HIV replication. High levels of HIV are found very soon after infection but then drop. Professor Levy said that a drop in CD8 cell activity precedes the loss of other immune system cells known as CD4 cells, which are a vital part of the body's defence against infection. HIV takes over these cells to replicate itself. It then destroys the CD4 cell.
Professor Levy said: 'We have shown that activity of CD8 cells is important for blocking replication of the Aids virus.' He said the new finding could explain why some people do not become infected with HIV despite repeated high risk behaviour. It is possible that the CD8 mechanism kills the virus very soon after infection. Why CD8 cells should lose this anti-HIV activity is not yet known.
The researchers also have isolated a protein, known as a cytokine, made by CD8 cells. It stops HIV replications in infected cells. They say they will completely purify the cytokine within six months, raising the possibility that it could be used as a drug.
Professor Levy's research has also highlighted the paradoxical role of antibodies in Aids. Antibodies are produced by the immune system. In HIV infection this antibody response declines. And in the later stages of Aids, the antibodies actually help HIV.
Because it replicates so rapidly HIV is constantly developing new genetic strains. By stopping replication CD8 also stops development of new mutants which are resistant to antibodies. 'Emphasis must be given to enhance this cellular immune response. It potentially can permit long-term survival of infected indivdiudals,' Professor Levy said.
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