A major mechanism of human immunodeficiency virus-induced cell killing does not involve cell fusion.

In vitro studies indicate that human immunodeficiency virus (HIV) infections are cytopathic for T4+ peripheral blood lymphocytes and for most continuous lines of T4+ lymphocytes. These cytopathic effects have been largely attributed to the formation of syncytia by HIV-infected cells. We report that HIV infections killed cultured peripheral blood lymphocytes and a line of T4+-lymphoid cells (CEM cells) without causing cell fusion. We also report that the occurrence of syncytia is an early and transitory phenomenon following infection of a fusion-susceptible line of T4+-cells (H9 cells). Mixing experiments and flow cytometry have been used to demonstrate that susceptibility to HIV-induced fusion is not determined by differences in presentation of viral envelope antigens or the surface levels of T4 receptor antigens on fusion-susceptible and -resistant cells. We conclude that a major mechanism of HIV-induced cell killing does not involve cell fusion and that HIV-induced cell fusion, when it does occur, requires factors in addition to viral envelope antigens and host T4 receptors.