Exposure of resting cd4 t-lymphocytes to HIV-1 upregulates l-selectin, the receptor for homing to lymph nodes, resulting in their sequestration from blood into lymph nodes

In vivo infection with HIV-1 eventually results in gradual depletion of CD4 T-lymphocytes in the blood, while for a certain time period T-lymphocytes increase in the lymph nodes (lymphoadenopathy, LAS). The reason for this phenomenon is not known. We found that exposure of resting T lymphocytes to HIV-1 transiently upregulated expression of cell surface CD62L (Lselectin), the receptor for homing to lymph nodes, which resulted in their enhanced binding (increased -12 fold, p < 0.001) to lymph node high endothelial venules (HEVs) in an imatta homing assay and their sequestration from the blood into lymph nodes following i.v. injection into SCID mice. This suggested that the decrease in numbers of CD4 T-lymphocytes in the blood of HIV-1 -infected subjects may reflect sequestration of abortively infected, resting T lymphocytes into lymph nodes rather than direct virus replication in and killing of these cells.