HIV Infected Adults In UCSF Study Show Evidence Of Thymu...( Contrary to the widely held belief th...)

HIV Infected Adults In UCSF Study Show Evidence Of Thymus Activity

Contrary to the widely held belief that the thymus -- an organ essential for producing competent immune cells -- is not functional in adulthood, researchers at the Gladstone Institute of Virology and Immunology have shown that half of the HIV-infected patients in a recent study appear to have substantial thymus function.

Thymus function in HIV-infected patients may mean that their bodies can compensate for the loss of T cells caused by HIV by re-awakening a dormant thymus and producing healthy T cells to fight off HIV infection. It also raises the possibility of therapies to replenish the immune system, by thymus stimulation or transplant, for those without a working thymus.

"Given the evidence that HIV can infect and destroy the thymus, this is an outcome that is not predicted by textbooks or clinical experience," said Joseph M. McCune, MD, PhD, associate professor of medicine at UC San Francisco, and an associate investigator at the UCSF-affiliated Gladstone Institute of Virology and Immunology, located at San Francisco General Hospital. McCune, who is the lead investigator of the study, said, "It is surprising not only that abundant thymic tissue could be found in these patients, but also that the percentage showing such tissue was so high."

"For patients over 40, it's a clear black and white difference, since in every uninfected individual over 40 that we looked at, we never saw thymus," he said. "Yet among those over 40 infected with HIV, five out of the ten had abundant thymus tissue."

Among the 99 HIV-positive patients in that study, the size of the thymus corresponded to the number of T cells circulating in the patient's blood, regardless of age: a larger thymus meant more T cells. All but one of the patients under 40 who were in the early stages of HIV disease progression had abundant thymic tissue, indicating that the thymus might be triggered into action by the first losses of T cells.

The research findings are reported in the June 1
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Contact: Mitzy Baker
mabaker@itsa.ucsf.edu
(415) 476-3804
University of California - San Francisco
3-Jun-1998

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