Altered expression of CD4, CD54, CD62L, and CCR5 in primary lymphocytes productively infected with the human immunodeficiency virus.

Infection of T cells with HIV-1 induces loss of CD4 and HLA class I from the cell surface. In the present article we have investigated whether changes in expression of other cell surface molecules could be related to HIV infection. To detect HIV-infected cells at the single-cell level, peripheral blood lymphocytes were infected in vitro with HIV-HSA, a reporter virus encoding the murine heat-stable antigen. Expression of HSA on activated primary lymphocytes was an efficient indicator of productive infection. Expression of the majority of the cell surface proteins studied was unaffected by HIV infection (HLA class I, II, CD11a, CD18, CD25, CD27, CD28, CD29, CD30, CD31, CD38, CD44, CD45R0, CD49d, CD57, CD94, CD95, and CXCR4). However, phenotypic changes specific to the productively infected cells were detected. Expression of the CD4 molecule was progressively lost and this was closely associated with loss of CD62L expression, a molecule involved in T cell homing into the lymph nodes. By contrast, T cells productively infected with this T-tropic reporter virus were enriched for CD54, and for CCR5, the main coreceptor for M-tropic viruses. Given the roles of CD62L, CD54, and CCR5 in lymphocyte trafficking, these results suggest that cells productively infected with HIV might have altered homing patterns in vivo.