4th International AIDS Society Conference on HIV Pathogenesis and Treatment


Sydney, Australia - July 22 - 25, 2007

PERSISTENT HIV-1 INFECTION IN DUODENAL MUCOSA AND MEMORY CD8+ T CELL DIFFERENTIATION

IAS Conf HIV Pathog Treat 2007 Jul 22-25;4th: Abstract No. MOAA101

Belmonte L.1, Zalar A.2, Bare P.3, Badano N.1, Araya V.2, Piskorz E.2, Figueroa M.I.4, Parodi C.1, Ruibal-Ares B.1, Cahn P.4, de Bracco M.M.1
1Academia Nacional de Medicina, Immunology, Buenos Aires, Argentina, 2Hospital Juan A Fernandez, Gastroenterology, Buenos Aires, Argentina, 3Academia Nacional de Medicina, Virology, Buenos Aires, Argentina, 4Hospital Juan A Fernandez, Infectology, Buenos Aires, Argentina

In order to identify the type of cells that harbour HIV-1 infection in the gut and the role of the effector immune response in this process, we studied 9 HIV+ and 8 HIV- controls (C). Fresh biopsies were collected from HIV+ and C. The presence of HIV-1 in the tissue was demonstrated by PCR and/or immunofluorecence (KC57 positivity). The phenotype of infiltrating cells in tissue was assessed by flow cytometry. CD4+ cells were depleted in the duodenal mucosa of HIV+ patients compared to C and CD4 reduction was not related to the presence of HIV-1 in the tissue (Mean+SD, HIV+:5.1+1.9% vs C:29.1+6.7%, p=0.006). In contrast, CD8+ T cells were elevated in HIV+ (HIV+:68.4+5% vs C:42+8%, p=0.02). To evaluate if HIV-1 infection of the mucosa could induce changes in the differentiation of CD8+T cells and if these could affect HIV-1 replication, we studied the expression of CD27 and CD28 on mucosal CD8+ T cells. The proportion of late memory effector CD8+ T cells (CD28-, CD27-) was not different in HIV+ and C. Likewise, the presence or not of HIV-1 in the tissue did not affect the expression of CD27 and CD28. Since CD4+ T lymphocytes were scarce in the duodenal mucosa of HIV-1 infected patients, we tried to identify the cells that sustained HIV-1 persistence in this tissue. HIV-1 infection of CD64+ mucosal macrophages was demonstrated by KC57 positivity, indicating that macrophages could be the source of continuous infection in this tissue. We had previously shown that HIV-1 persistence in the duodenal mucosa was independent of the efficacy of HAART (negativization of plasma viral load and blood CD4 count recovery). Since HAART may not be fully effective to interfere with HIV-1 replication in macrophages, it will be important to assess the role of these cells in the gut as reservoirs of HIV infection.

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2007-07-22
MOAA101
Immune Activation in HIV Pathogenesis

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