Quantitative Study of beta 1 -Integrin Expression and Fibronectin Interaction Profile of T Lymphocytes in Vitro Infected with HIV

Abstract

Cell-extracellular matrix interactions, regulated in part by beta₁-integrins, play a key role in the recirculation of T lymphocytes and tissue infiltration in inflammatory and immune responses. HIV infection may affect CD4⁺ T cell adhesion, and the trafficking and migration of these cells, which are crucial for foreign antigen recognition. We investigated this by studying the expression of the beta₁-integrin chains CD29 and CD49c,-d, -e, and-f, on in vitro HIV-infected primary T cells. We also assessed fibronectin binding and production by CD4⁺ lymphocytes. X4 (HIV-1/LAI), R5 (HIV-1/Ba-L), and X4R5 (HIV-2/ROD) strains, and X4R5 primary isolates (HIV-1/DAS, HIV-1/THI), with different cytopathogenicity and replication kinetics, were used. beta₁-integrin expression on CD4⁺ and CD4^- T cell subpopulations was regulated by cell activation with phytohemagglutinin-P and interleukin 2, but was unaffected by HIV infection, even at the peak of viral replication and CD4⁺ cell depletion. Similarly, fibronectin binding to CD4⁺ lymphocytes was not affected by HIV infection. This suggests that infected lymphocytes may be able to extravasate, migrate, and recirculate within the body until their death.