AIDSWEEKLY Plus, Monday, 24 March 1997
Daniel J. DeNoon, Senior Editor
HIV evades the human immune system by quickly evoking elimination of virus-specific T cell clones.
This phenomenon does not occur during infection with Epstein-Barr virus (EBV), another chronic viral infection.
Cecilia Graziosi and colleagues from Anthony S. Fauci's laboratory at the National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, announced the findings during a late-breaker session of the Fourth Conference on Retroviruses and Opportunistic Infections, held January 22-26 in Washington, D.C.
"Rapid deletion of virus-specific T cell clones occurred in HIV but not in EBV infection," they wrote in their presentation abstract. "This ... phenomenon may represent an important mechanism of HIV escape from the immune response."
Graziosi et al. studied the clonal expansion patterns of V(beta) T cell subsets during the primary immune response to either HIV-1 or EBV infection. They then correlated these patterns with concurrent patterns of cytokine expression.
Contrary to expectation, HIV evaded T cell-mediated immunity not by developing mutations in T cell epitopes but by somehow causing the disappearance of HIV specific T cells.
"A significant number of HIV specific T cell clones involved in the primary immune response to HIV rapidly declined or disappeared during primary infection or following transition to the chronic phase, in the absence of mutations in the virus epitopes recognized by these clones," Graziosi et al. wrote.
This was not the case for EBV infection: dominant EBV specific T cell clones remained present throughout primary infection and remained detectable after clinical resolution of the infection.
Cytokine expression was similar in both primary HIV-1 and EBV infection. There was little or no peripheral blood mononuclear cell (PBMC) expression of interleukin 2 (IL-2) or IL-4. However, there was consistent expression of IL-10, tumor necrosis factor alpha (TNF-(alpha)), and interferon gamma (IFN-gamma).
Interestingly, IFN-gamma expression peaked coincidentally with oligoclonal CD8(+) T cell expansions in five patients with primary HIV infection and in two patients with primary EBV infection.
"These results indicate that high levels of expression of proinflammatory cytokines are associated with both HIV and EBV primary infections," Graziosi et al. wrote.
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