September 24, 2007
A sudden loss of T cells (white blood cells crucial to the immune system) is not the trigger for the onset of AIDS, according to a study published in the September 1, 2007 issue of the Journal of Immunology by a team of researchers at Tulane National Primate Research Center. The study, "Acute Loss of Intestinal CD4+ T Cells is Not Predictive of Simian Immunodeficiency Virus Virulence," challenges current thinking regarding AIDS, namely that a sudden, acute loss of T cells is considered to be sufficient to predict progression to the disease's last stages: final collapse of the immune system and death.
The team, led by Ivona V. Pandrea and Cristian Apetrei of Tulane University, states that although a severe acute depletion of T cells was previously considered to trigger progression to full-blown AIDS in humans, some non-human primates infected with simian immunodeficiency virus (SIV) do not develop AIDS after such a depletion. African green monkeys infected with SIV, for example, were found to recover even after a period of severe T cell depletion.
Two companion papers in the Journal of Immunology by researchers from the University of Pennsylvania and Southwestern University of Dallas came to the same conclusions in their studies of sooty mangabeys.
Another major question raised by the study is why monkeys with SIV, unlike HIV-positive humans, are generally resistant to progression to AIDS after infection with the virus. The answer, the authors propose, is that thousands of years of host/virus co-adaptation has enabled monkeys, the natural hosts of SIV, to effectively limit T cell immune activation and apoptosis, a mechanism that leads to progression of the disease. By contrast, humans, who were introduced to the virus relatively recently, have not had the opportunity to develop such protective adaptations.
The authors also suggested that approaches to control immune system activation and resultant cell death should be considered for use in addition to currently available therapies to slow progression of the disease in HIV-infected individuals.
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