Salmonella typhimurium-induced reactivation of latent HIV-1 in promonocytic U1 cells is inhibited by trovafloxacin.
We have previously reported that virulent Salmonella typhimurium induces replication of latent HIV-1 in U1 cells, via activation of tumor necrosis factor-alpha (TNF-alpha) production. In the present study, we show that Trovafloxacin, a new quinolone antibiotic, inhibits S. typhimurium-induced TNF-alpha production and HIV-1 replication. In addition, Trovafloxacin inhibits TNF-alpha-induced reactivation of latent HIV-1 in U1 cells. The concentrations of Trovafloxacin that inhibited HIV-1 replication are comparable to the plasma and tissue levels achieved by therapeutic dosage used in the treatment of bacterial infections. Therefore, Trovafloxacin is a potential candidate for adjunct therapy in HIV-1 infection.
Gollapudi
S
S
Division of Basic and Clinical Immunology, Dept Medicine, University of California Irvine 92697, USA.
Gupta
S
S
Thadepalli
H
H
D000890:Anti-Infective Agents / Q000494:pharmacology*; D024841:Fluoroquinolones; D015497:HIV-1 / Q000187:drug effects* / Q000254:growth & development / Q000502:physiology; D006801:Humans; D007424:Intracellular Fluid / Q000382:microbiology; D009000:Monocytes / Q000166:cytology; D009287:Naphthyridines / Q000494:pharmacology*; D012486:Salmonella typhimurium / Q000187:drug effects* / Q000254:growth & development; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D020298:U937 Cells; D014775:Virus Activation / Q000187:drug effects*; D017735:Virus Latency; D014779:Virus Replication / Q000187:drug effects
D000890:Anti-Infective Agents; D024841:Fluoroquinolones; D009287:Naphthyridines; D014409:Tumor Necrosis Factor-alpha; C080163:trovafloxacin