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Second pathway behind HIV-associated immune system dysfunction identified
Date:9/30/2007

cipants whose immune systems were naturally able to suppress HIV replication without antiviral medications elite controllers in whom viral levels are too low to be detected.

Elevated CTLA-4 expression also correlated with signs of disease progression increased viral load and reduced overall CD4 count. While antiviral treatment caused viral loads to drop significantly after treatment began, it resulted in only modest and slow drops in CTLA-4 expression. In vitro tests of the effects of blocking the CTLA-4 molecule improved the function of HIV-specific CD4 cells. Comparing the effects of blocking CTLA-4 with those of blocking PD-1 or both molecules produced functional improvements that varied considerably between participants, signifying a complex relationship between the pathways controlled by the two molecules.

Both of these pathways contribute to dysfunction of HIV-specific T cells and both may be considered targets for therapeutic intervention. But since their mechanisms are so complicated, further study is needed before clinical trials can be planned, says Kaufmann, an instructor in Medicine at Harvard Medical School (HMS).

Understanding why the immune system fails to control HIV is essential for development of vaccines and new therapies said Bruce Walker, MD, director of PARC-MGH and senior author of the study. These studies suggest that the immune system is turning itself off prematurely in HIV-infected persons, and the big challenge now is to figure out if we can turn it back on, getting it to do what it is supposed to do, without causing collateral damage in the process. Walker is a professor of Medicine at HMS and a Howard Hughes Medical Institute (HHMI) investigator.


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Contact: Sue McGreevey
smcgreevey@partners.org
617-724-2764
Massachusetts General Hospital
Source:Eurekalert

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