Inhibition of human immunodeficiency virus type 1 replication prior to reverse transcription by influenza virus stimulation

It is now recognized that, in addition to drug-mediated therapies against h uman immunodeficiency virus type 1 (HIV-1), the immune system can exert ant iviral effects via CD8(+) T-cell-generated anti-HIV factors. This study dem onstrates that (i) supernatants from peripheral blood mononuclear cells (PB MC) stimulated with influenza A virus inhibit replication of CCR5- and CXCR 4-tropic HIV-1 isolates prior to reverse transcription; (ii) the HIV-suppre ssive supernatants can be generated by CD4- or CD8-depleted PBMC; (iii) thi s anti-HIV activity is partially due to alpha interferon (IFN-alpha), but n ot to IFN-gamma, IFN-beta, the beta-chemokines MIP-1 alpha, MIP-1 beta, and RANTES, or interleukin-16; (iv) the anti-HIV activity is generated equally well by PBMC cultured with either infectious or UV-inactivated influenza A virus; and (v) the antiviral activity can be generated by influenza A-stim ulated PBMC from HN-infected individuals. These findings represent a novel mechanism for inhibition of HIV-1 replication that differs from the previou sly described CD8 anti-HIV factors (MIP-la, MIP-1 beta, RANTES, and CD8 ant iviral factor).