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Factors associated with collagen deposition in lymphoid tissue in long-term treated HIV-infected patients

2010; Lippincott Williams & Wilkins; Volume: 24; Issue: 13 Linguagem: Inglês

10.1097/qad.0b013e32833c3268

1473-5571

Alba Díaz, Llúcia Alós, Agathe León, Anna Mozos, Miguel Caballero, Antonio Martı́nez, Montserrat Plana, Teresa Gallart, Cristina Gil, Manuel Leal, José M. Gatell, Felipe García,

HIV/AIDS oral health manifestations

Objective: The factors associated with fibrosis in lymphoid tissue in long-term treated HIV-infected patients and their correlation with immune reconstitution were assessed. Methods: Tonsillar biopsies were performed in seven antiretroviral-naive patients and 29 successfully treated patients (median time on treatment, 61 months). Twenty patients received protease inhibitors-sparing regimens and nine protease inhibitor-containing regimens. Five tonsillar resections of HIV-negative individuals were used as controls. Lymphoid tissue architecture, collagen deposition (fibrosis) and the mean interfollicular CD4+ cell count per μm2 were assessed. Results: Naive and long-term treated HIV-infected patients had a higher proportion of fibrosis than did HIV-uninfected persons (P < 0.001). Patients with greater collagen deposition showed lower levels of CD4+ cells in lymphoid tissue (P = 0.03) and smaller increase in peripheral CD4+ T cells (r = −0.40, P = 0.05). The factors independently associated with fibrosis in lymphoid tissue were age (P < 0.0001), treated patients with detectable lymphoid tissue viral load when compared with patients with undetectable lymphoid tissue viral load (median 5 vs. 12%, respectively, P = 0.017) and patients receiving a protease inhibitor-sparing vs. a protease inhibitor-containing regimen (median 8 vs. 2.5%, respectively, P = 0.04). Conclusion: Fibrosis in lymphoid tissue was associated with a poor reconstitution of CD4+ T cells and long-term antiretroviral therapy did not reverse this abnormality. HIV infection, older age, a detectable level of lymphoid tissue viral load in treated patients and protease inhibitor-sparing regimens seem to favour fibrosis in lymphoid tissue.