The Spontaneous Control of HIV Replication is Characterized by Decreased Pathological Changes in the Gut-associated Lymphoid Tissue

• Published in: Current HIV research Vol. 16; no. 5; p. 338
• Main Authors: Taborda, Natalia A, Correa, Luis A, Feria, Manuel Geronimo, Rugeles, María T
• Format: Journal Article
• Language: English
• Published: Netherlands 01.01.2018
• Subjects: histopathological alterations; GALT; CD4+ T cells; Noncontrollers; rectosigmoidoscopy; HIV-controllers
• ISSN: 1873-4251
• DOI: 10.2174/1570162X17666190130115113

HIV infection induces alterations in the gut-associated lymphoid tissue (GALT) that constitutes the most important site for viral replication due to the extensive presence of effector memory T-cells. In the case of HIV-controllers, several studies have reported fewer peripheral alterations and conserved immune responses that correlate with viral control; however, the histopathological characterization of GALT in those patients is still missing. In this study, we evaluated pathological alterations in GALT, trying to associate them with clinical parameters of HIV infected patients with or without evidence of viral control. This study included eight HIV-controllers (antiretroviral treatment-naïve patients, with viral loads below 2.000 copies/mL for at least 1 year); 14 Noncontrollers (antiretroviral treatmentnaïve patients, with viral loads > 2.000 copies/mL and CD4+ T cells count > 250 cells/μL), and 12 uninfected donors. Biopsy fragments were obtained by rectosigmoidoscopy and stained with hematoxylin and eosin, silver methenamine, Ziehl Neelsen, and modified Ziehl Neelsen. Histopathological findings in HIV-controllers were similar to those observed in the uninfected group. In contrast, noncontrollers exhibited several alterations including condyloma acuminate, squamous metaplasia and acute colitis. These alterations were associated with disease progression. HIV-controllers exhibit lower pathological alterations in the gut tissue, associated with higher CD4 T cell count, and lower viral load.