Alternative complement pathway activation by HIV infected cells: C3 fixation does not lead to complement lysis but enhances NK sensitivity.

HIV infected T and monocytic cell lines could activate and fix C3 fragments when incubated in human serum under conditions allowing for activation of the alternative complement pathway. Normal T lymphocytes incubated with HIV could also activate and fix C3. This activity was, at least in part, the property of the virus itself since cell-free HIV could efficiently activate C3. The C3 activating HIV infected cells were resistant to complement-mediated lysis, even after prolonged incubation periods. However, their sensitivity to cell-mediated natural killing increased, presumably due to their interaction with complement receptor bearing NK lymphocytes. The results suggest that the alternative complement pathway may contribute to the depletion of CD4+ T lymphocytes during HIV infection in vivo.