4th Conference on Retroviruses and Opportunistic Infections Washington, DC - January 22-26, 1997

Conf Retroviruses Opportunistic Infect 1997 Jan 22-26; 4th:71 (abstract no. 33)

Angel JB, Parato K, Kumar A, Filion LG, Diaz-Mitoma F, Pham B, Sun E, Leonard J, Cameron DW; Ottawa General Hospital, Ottawa, Ontario, Canada.

Background: Loss of cell mediated immunity (CMI) leads to the development of HIV related opportunistic infections and the inability to restrict HIV replication.

Methods: We investigated the effect of potent antiretroviral therapy (ritonavir plus saquinavir) on several functional measures of CMI in HIV-infected patients with 100-500 CD4+ T cells/µL . Proliferative responses to PHA, p24 Ag and tetanus toxoid (TT), as well as IL-2, IL-12 and IL-10 production were measured at baseline, 4 and 24 weeks and correlated with changes in viral load and CD4+ T cell count.

Results: Median decrease in plasma viral load was greater than 2 log₁₀ at 4 wks and greater than 4 log₁₀ at 12 wks. At 4 wks, proliferative responses to PHA, p24 Ag and TT developed or improved in 27/41, 14/41 and 3/8 patients respectively. Cytokine data is tabulated: (Table: see text) A dramatic (greater than 8-fold) increase in the response to PHA correlated with a greater CD4+ T cell rise (P=0.0075). Data collected at 24 wks is being similarly analyzed.

Conclusion: These data illustrate an immunologic effect of potent anti-HIV therapy which appears rapidly with the onset of antiviral effect, suggesting that HIV-induced functional immune suppression is dynamic and potentially reversible.

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Copyright © 1980, 1997 - Foundation for Retrovirology and Human Health. Reproduction of this abstract (other than one copy for personal reference) must be cleared through the Foundation for Retrovirology and Human Health. Licensed through AIDSLINE, National Library of Medicine.