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.
Scheglovitova
O
O
Gamaleya Institute for Microbiology and Epidemiology, Moscow, Russia.
Ershov
F
F
D002460:Cell Line; D002478:Cells, Cultured; D004727:Endothelium / Q000166:cytology; D015497:HIV-1 / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism; D006801:Humans; D012330:RNA, Double-Stranded / Q000494:pharmacology*; D012331:RNA, Fungal / Q000494:pharmacology*; D013601:T-Lymphocytes / Q000166:cytology / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014471:Umbilical Veins / Q000166:cytology / Q000378:metabolism*
D012330:RNA, Double-Stranded; D012331:RNA, Fungal; D014409:Tumor Necrosis Factor-alpha; C076741:ridostin