The proteinase inhibitor pepstatin A inhibits formation of reverse transcriptase in H9 cells infected with human immunodeficiency virus 1.
Retroviruses depend on a virus-encoded proteinase. As this enzyme is an interesting target for antiviral therapy, we examined the effect of various low-molecular-weight proteinase inhibitors, as well as a few oligopeptides related to the proteolytic cleavage sites, on the replication of HIV-1 in H9 cells. The increase in reverse transcriptase activity during incubation was assumed to reflect viral replication. Cellular DNA synthesis was measured to quantitate the adverse effects of the inhibitors on the cells. Only one of the substances tested, pepstatin A, had an appreciable selective effect on viral replication. Substances that decreased DNA synthesis generally caused an equally large decrease in reverse transcriptase activity.
Grinde
B
B
Department of Virology, National Institute of Public Health, Oslo, Norway.
Hungnes
O
O
Tjøtta
E
E
D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology; D002460:Cell Line; D004279:DNA, Viral / Q000096:biosynthesis; D015497:HIV-1 / Q000187:drug effects / Q000201:enzymology* / Q000502:physiology; D006801:Humans; D009842:Oligopeptides / Q000494:pharmacology*; D010436:Pepstatins / Q000494:pharmacology*; D012194:RNA-Directed DNA Polymerase / Q000096:biosynthesis; D018894:Reverse Transcriptase Inhibitors; D014779:Virus Replication / Q000187:drug effects
D004279:DNA, Viral; D009842:Oligopeptides; D010436:Pepstatins; D018894:Reverse Transcriptase Inhibitors; C014195:Streptomyces pepsin inhibitor; D012194:RNA-Directed DNA Polymerase; C031375:pepstatin