Scientists Find New Clues to How HIV Avoids Host..

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Scientists Find New Clues to How HIV Avoids Host Immune Response

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WESTPORT, CT (Reuters) Nov 30 - High levels of HIV replication suppress the ability of circulating HIV-specific CD4+ T cells to develop an anti-HIV proliferative response, according to new research published in the November 20th issue of the Proceedings of the National Academy of Sciences. The findings offer new clues to how HIV avoids destruction by a host immune response.



"The results show that HIV viremia moderately diminishes responses to non-HIV antigens but profoundly diminishes the proliferative response to HIV," study director Dr. Mark Connors, of the National Institutes of Health, in Bethesda, Maryland, told Reuters Health.



Dr. Connors and colleagues examined levels and proliferation of HIV-specific CD4+ T cells in a cohort of 26 HIV-1-infected patients who were not receiving antiretroviral therapy. While they were able to detect HIV-specific CD4+ T cells capable of producing interferon-gamma in the patients, proliferative responses to HIV were absent.



"In a separate cohort, interruption of antiretroviral therapy resulted in the rapid and complete abrogation of virus-specific proliferation although HIV-1-specific CD4+ T cells were present," the investigators explain in the journal. Proliferation of HIV-specific CD4+ T cells returned with the resumption of treatment and viremic control.



The study findings have several important implications for clinical practice, Dr. Connors explained. "Interrupting therapy does not boost HIV-specific proliferative responses." In fact, the opposite occurs, indicating that treatment interruption is not an effective way to boost the HIV-specific immune response.



HIV-specific CD4+ T cells are not deleted as previously thought and likely can be boosted, Dr. Connors told Reuters Health. In fact, his group was able to induce a proliferative response to HIV in viremic patients in vitro using costimulation with anti-CD28 antibody.



The maintenance of a proliferative response to HIV did not predict long-term viremic control. This means that "the absence of proliferation or low numbers of HIV-specific CD4s are not the critical defect in progressors," Dr. Connors explained.



Proc Natl Acad Scie USA 2001;98:13878-13883.





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