Molecular bases for the anti-HIV-1 effect of NO. Commentary.
In infected human cells, nitric oxide (NO) has been shown to inhibit the replication of the human immunodeficiency virus-1 (HIV-1), the etiological agent of AIDS. Evidence suggests that NO may regulate HIV-1 replication by affecting the sulphydryl redox state. In this respect, it has been very recently demonstrated that NO-donors inactivate the HIV-1-encoded protease and reverse transcriptase in vitro. Further viral and host NO targets may be envisaged. Although no data are available on the anti-HIV-1 effect of NO in vivo, NO-releasing drugs, clinically used in the treatment of cardiovascular disorders, may represent a novel class of molecules for decreasing virus replication. Here, the possible molecular bases for the anti-HIV-1 effect of NO are discussed.
Persichini
T
T
Department of Biology, University of Rome <Roma Tre>, I-00146 Rome, Italy.
Ascenzi
P
P
Colizzi
V
V
Fraziano
M
M
Venturini
G
G
Colasanti
M
M
D000163:Acquired Immunodeficiency Syndrome / Q000188:drug therapy / Q000821:virology*; D019427:HIV Integrase / Q000737:chemistry / Q000502:physiology; D016333:HIV Protease / Q000737:chemistry / Q000502:physiology; D054303:HIV Reverse Transcriptase / Q000737:chemistry / Q000502:physiology; D015497:HIV-1 / Q000737:chemistry / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D009569:Nitric Oxide / Q000737:chemistry / Q000502:physiology*; D020030:Nitric Oxide Donors / Q000494:pharmacology / Q000627:therapeutic use; D014779:Virus Replication / Q000187:drug effects / Q000502:physiology*
D020030:Nitric Oxide Donors; D009569:Nitric Oxide; D019427:HIV Integrase; D054303:HIV Reverse Transcriptase; D016333:HIV Protease