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HIV infection of primary cells involves crosstalk between HIV proteins and host cell proteins. Recent work has shown that cell apoptosis is induced following the exposure of cells to multiple viral proteins including Tat, gp120, and Nef. This apoptosis may be responsible for eliminating T cells that are infected with HIV and establishing a reservoir of uninfected cells. However, the majority of HIV-infected T cells in infected individuals are relatively resistant to this apoptosis, suggesting that some antiapoptotic mechanism of HIV-1 may exist. Fas ligand (FasL) is a cell surface molecule and a potent inducer of apoptosis in many cell types. In this report, we show that FasL is present on HIV-infected T cells and co-localizes with Tat protein and viral RNA in the cytoplasm of HIV-infected cells. The induction of FasL in HIV-infected cells could be directly regulated by HIV Tat. As a downstream signal, we found that HIV Tat induces the activation of NF-kappaB, resulting in the induction of FasL expression in HIV-infected cells. Our results show that HIV-1 viral proteins, especially Tat, can induce FasL expression in the infected cells via NF-kappaB activation. This study indicates that HIV Tat may be able to modulate
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