Ridostin inhibits transfer of HIV-1 from abortively infected human umbilical vein endothelial cells to T lymphoblastoid cells.

The exposure of human umbilical vein endothelial (HUVE) cells to Ridostin resulted in reduced extent of virus rescue after the addition of indicator T cells. The inhibitory effect was accompanied by decreased synthesis of tumor necrosis factor (TNF) alpha by HUVE cells. The reduced TNF alpha synthesis caused by Ridostin treatment could be responsible, at least in part, for the inhibition of human immunodeficiency virus 1 (HIV-1) infection in our experimental system, at multiple steps of this process, such as: infection of HUVE cells, transfer to and subsequent replication in rescuing cells.

Ridostin inhibits HIV-1 replication in the T lymphoblastoid cell line C8166. Possible role of altered cytokine production.

Altered cytokine production in human immunodeficiency virus 1 (HIV-1) infection is well documented and cytokine modulators are currently under investigation as possible therapeutic agents. We tested the ability of Ridostin (dsRNA preparation derived from S. cervisiae) to inhibit HIV-1 replication in acutely infected T lymphoblastoid C8166 cells.

Antibody to ICAM-1 mediates enhancement of HIV-1 infection of human endothelial cells.

Human umbilical vein endothelial cells (HUVEC) can be abortively infected with HIV-1, but virus production is rescued by the addition of T cells. Monoclonal antibody (Mab) to ICAM-1, but not its Fab' fragment or MAbs to LFA-1 and PECAM-1, increases HIV-1 infection of HUVEC by enhancing HIV-1 absorption. Enhancement by anti ICAM-1 is probably due to a bridging effect different from the ADE mediated by anti-gp120 that involves FcR or CR-mediated capture of the virus-antibody complex.