Human immunodeficiency virus type 2 produces a defect in CD3-gamma gene transcripts similar to that observed for human immunodeficiency virus type 1.

T cells are central players in the immune response to infectious disease, with the specificity of their responses controlled by the T-cell receptor (TCR)/CD3 complex on the cell surface. Impairment of TCR/CD3-directed CD4(+) T-cell immune responses is frequently observed in individuals infected with human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2). Virus replication is also regulated by T-cell activation factors, with HIV-1 and HIV-2 responding to different TCR/CD3-directed cellular pathways.

Modulation of CD3-gamma gene expression after HIV type 1 infection of the WE17/10 T cell line is progressive and occurs in concert with decreased production of viral p24 antigen.

HIV-1 infection of WE17/10, an IL-2-dependent CD4+ human T cell line, abrogates T cell receptor (TCR)/CD3 expression due to a transcription level defect in the CD3-gamma chain gene. Kinetic examination of surface receptor density reveals that these complexes are progressively reduced early after HIV-1 infection as the cells transition from TCR/CD3hi-->TCR/CD3lo-->TCR/CD3-. The passage from TCR/CD3hi reversible TCR/CD3lo is characterized by a steady decrease in receptor density from 100 to 50% of control values with similar kinetic for all of the viral variants tested.