In infected human cells, nitric oxide (NO) has been shown to inhibit the re
plication of the human immunodeficiency virus-1 (HIV-1), the etiological ag
ent of AIDS. Evidence suggests that NO may regulate HIV-1 replication by af
fecting the sulphydryl redox state. In this respect, it has been very recen
tly demonstrated that NO-donors inactivate the HIV-1-encoded protease and r
everse transcriptase in vitro. Further viral and host NO targets may be env
isaged. Although no data are available on the anti-HIV-1 effect of NO in vi
vo, NO-releasing drugs, clinically used in the treatment of cardiovascular
disorders, may represent a novel class of molecules for decreasing virus re
plication. Here, the possible molecular bases for the anti-HIV-1 effect of
NO are discussed.