Retroviral interference on STAT activation in individuals coinfected with human T cell leukemia virus type 2 and HIV-1.

Human T cell leukemia virus (HTLV) type-2 is a human retrovirus whose infection has not been tightly linked to human diseases. However, the fairly high prevalence of this infection among HIV-1-positive individuals indicates the importance of better understanding the potential interference of HTLV-2 infection on HIV-1 infection and AIDS. We previously demonstrated that one signature of PBMC freshly derived from HIV-1-infected individuals is the constitutive activation of a C-terminal truncated STAT5 (STAT5Delta).

Urokinase-urokinase receptor interaction mediates an inhibitory signal for HIV-1 replication.

Elevated levels of soluble urokinase-type plasminogen activator (uPA) receptor, CD87/u-PAR, predict survival in individuals infected with HIV-1. Here, we report that pro-uPA (or uPA) inhibits HIV-1 expression in U937-derived chronically infected promonocytic U1 cells stimulated with phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-alpha (TNF-alpha). However, pro-uPA did not inhibit PMA or TNF-alpha-dependent activation of nuclear factor-kB or activation protein-1 in U1 cells.