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Developing an AIDS Vaccine

In the decade since the recognition of the first cases of AIDS, the firs disease has grown into one of the leading causes of death in the world. Despite rapid progress in isolating and identifying the human immunodeficiency virus (HIV), it is still not clear what causes the collapse of the immune system that makes its victims so vulnerable to opportunistic infections. One thing is clear-although the target for HIV infection is the helper T cell, most helper T cells are not infected with the virus. The destruction of these cells as the disease progresses, therefore, must have another cause.

Several proposals have recently been advanced to explain the ultimate destruction of uninfected T cells. One of these proposals suggests that infection with HIV triggers an autoimmune response-that is , the body begins to mount an attack against its own T cells. Another proposal suggests that HIV acts as a super antigen, stimulating immune cells to respond to the antigen but to respond in a way that ultimately leads to their own death. The HIV antigens might be encouraging immune cells to commit suicide.
Proponents to the autoimmune hypothesis point to experiments performed in uninfected mice immunized with normal lymphocytes from another strain of uninfected mice. After exposure to foreign lymphocytes, the immunized mice produced antibodies to the HIV envelope protein gp 120. This suggests that gp 120 and a lymphocyte antigen share some common properties. Antibodies formed against HIV cross-react with the host’s lymphocytes and destroy them. If this is true, it has frightening implications for the hoped-for vaccine against AIDS. A vaccine that stimulates antibody to gp 120 could itself trigger an AIDS-like paralysis of the immune system.
Other researchers have uncovered evidence that HIV can act as a super antigen. Such molecule bind to T-cell receptors in an unusual manner-they need only recognized a portion of the receptor in order to activate the T cells. Super antigens bypass the specificity required of most antigens and activate diverse populations of T cells. Worse T cells stimulated by super antigens are programmed for death, so the disease is already progressing before the actual loss of T cells is measurable. If the pathology of AIDS is due to a super antigen then any antiviral therapy would have to be early enough in the infections to prevent exposure of most T cells to the antigen. Like the first proposal. This pathogenic mechanism could seriously impair the development of a development of a suitable vaccine.

If either these scenarios is true, any super antigens or cross-reacting antigens would have to be identified and meticulously excluded from the vaccine. 
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