StressCovidV1, PubMed, Curation, bibRecord, 000933

Nitric oxide as an endogenous mutagen for Sendai virus without antiviral activity.

Identifieur interne : 000933 ( PubMed/Curation ); précédent : 000932; suivant : 000934

Nitric oxide as an endogenous mutagen for Sendai virus without antiviral activity.

Auteurs : Jun Yoshitake [Japon] ; Takaaki Akaike ; Teruo Akuta ; Fumio Tamura ; Tsutomu Ogura ; Hiroyasu Esumi ; Hiroshi Maeda

Source :

Journal of virology [ 0022-538X ] ; 2004.

RBID : pubmed:15280479

Descripteurs français

KwdFr :
- Animaux, Composés nitrés (métabolisme), Guanosine (analogues et dérivés), Guanosine (métabolisme), Humains, Lignée cellulaire, Monoxyde d'azote (pharmacologie), Mutagènes (pharmacologie), Mutation (), Nitric oxide synthase (génétique), Nitric oxide synthase (métabolisme), Nitric oxide synthase type II, Protéines luminescentes (génétique), Protéines luminescentes (métabolisme), Protéines à fluorescence verte, Réplication virale, Souris, Stress oxydatif, Virus Sendai (), Virus Sendai (génétique), Virus Sendai (métabolisme).
MESH :
- analogues et dérivés : Guanosine.
- génétique : Nitric oxide synthase, Protéines luminescentes, Virus Sendai.
- métabolisme : Composés nitrés, Guanosine, Nitric oxide synthase, Protéines luminescentes, Virus Sendai.
- pharmacologie : Monoxyde d'azote, Mutagènes.
- Animaux, Humains, Lignée cellulaire, Mutation, Nitric oxide synthase type II, Protéines à fluorescence verte, Réplication virale, Souris, Stress oxydatif, Virus Sendai.

English descriptors

KwdEn :
- Animals, Cell Line, Green Fluorescent Proteins, Guanosine (analogs & derivatives), Guanosine (metabolism), Humans, Luminescent Proteins (genetics), Luminescent Proteins (metabolism), Mice, Mutagens (pharmacology), Mutation (drug effects), Nitric Oxide (pharmacology), Nitric Oxide Synthase (genetics), Nitric Oxide Synthase (metabolism), Nitric Oxide Synthase Type II, Nitro Compounds (metabolism), Oxidative Stress, Sendai virus (drug effects), Sendai virus (genetics), Sendai virus (metabolism), Virus Replication.
MESH :
- chemical , analogs & derivatives : Guanosine.
- chemical , genetics : Luminescent Proteins, Nitric Oxide Synthase.
- chemical , metabolism : Guanosine, Luminescent Proteins, Nitric Oxide Synthase, Nitro Compounds.
- chemical , pharmacology : Mutagens, Nitric Oxide.
- chemical : Green Fluorescent Proteins, Nitric Oxide Synthase Type II.
- drug effects : Mutation, Sendai virus.
- genetics : Sendai virus.
- metabolism : Sendai virus.
- Animals, Cell Line, Humans, Mice, Oxidative Stress, Virus Replication.

Abstract

Nitric oxide (NO) may affect the genomes of various pathogens, and this mutagenesis is of particular interest for viral pathogenesis and evolution. Here, we investigated the effect of NO on viral replication and mutation. Exogenous or endogenous NO had no apparent antiviral effect on influenza A virus and Sendai virus. The mutagenic potential of NO was analyzed with Sendai virus fused to a green fluorescent protein (GFP) gene (GFP-SeV). GFP-SeV was cultured in SW480 cells transfected with a vector expressing inducible NO synthase (iNOS). The mutation frequency of GFP-SeV was examined by measuring loss of GFP fluorescence of the viral plaques. GFP-SeV mutation frequency in iNOS-SW480 cells was much higher than that in parent SW480 cells and was reduced to the level of mutation frequency in the parent cells by treatment with an NO synthase (NOS) inhibitor. Immunocytochemistry showed generation of more 8-nitroguanosine in iNOS-SW480 cells than in SW480 cells without iNOS transfection. Authentic 8-nitroguanosine added exogenously to GFP-SeV-infected CV-1 cells increased the viral mutation frequency. Profiles of the GFP gene mutations induced by 8-nitroguanosine appeared to resemble those of mutations occurring in mouse lungs in vivo. A base substitution that was characteristic of both mutants (those induced by 8-nitroguanosine and those occurring in vivo) was a C-to-U transition. NO-dependent oxidative stress in iNOS-SW480 cells was also evident. Together, the results indicate unambiguously that NO has mutagenic potential for RNA viruses such as Sendai virus without affecting viral replication, possibly via 8-nitroguanosine formation and cellular oxidative stress.

DOI: 10.1128/JVI.78.16.8709-8719.2004
PubMed: 15280479

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Le document en format XML

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<front><div type="abstract" xml:lang="en">Nitric oxide (NO) may affect the genomes of various pathogens, and this mutagenesis is of particular interest for viral pathogenesis and evolution. Here, we investigated the effect of NO on viral replication and mutation. Exogenous or endogenous NO had no apparent antiviral effect on influenza A virus and Sendai virus. The mutagenic potential of NO was analyzed with Sendai virus fused to a green fluorescent protein (GFP) gene (GFP-SeV). GFP-SeV was cultured in SW480 cells transfected with a vector expressing inducible NO synthase (iNOS). The mutation frequency of GFP-SeV was examined by measuring loss of GFP fluorescence of the viral plaques. GFP-SeV mutation frequency in iNOS-SW480 cells was much higher than that in parent SW480 cells and was reduced to the level of mutation frequency in the parent cells by treatment with an NO synthase (NOS) inhibitor. Immunocytochemistry showed generation of more 8-nitroguanosine in iNOS-SW480 cells than in SW480 cells without iNOS transfection. Authentic 8-nitroguanosine added exogenously to GFP-SeV-infected CV-1 cells increased the viral mutation frequency. Profiles of the GFP gene mutations induced by 8-nitroguanosine appeared to resemble those of mutations occurring in mouse lungs in vivo. A base substitution that was characteristic of both mutants (those induced by 8-nitroguanosine and those occurring in vivo) was a C-to-U transition. NO-dependent oxidative stress in iNOS-SW480 cells was also evident. Together, the results indicate unambiguously that NO has mutagenic potential for RNA viruses such as Sendai virus without affecting viral replication, possibly via 8-nitroguanosine formation and cellular oxidative stress.</div>
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<Abstract><AbstractText>Nitric oxide (NO) may affect the genomes of various pathogens, and this mutagenesis is of particular interest for viral pathogenesis and evolution. Here, we investigated the effect of NO on viral replication and mutation. Exogenous or endogenous NO had no apparent antiviral effect on influenza A virus and Sendai virus. The mutagenic potential of NO was analyzed with Sendai virus fused to a green fluorescent protein (GFP) gene (GFP-SeV). GFP-SeV was cultured in SW480 cells transfected with a vector expressing inducible NO synthase (iNOS). The mutation frequency of GFP-SeV was examined by measuring loss of GFP fluorescence of the viral plaques. GFP-SeV mutation frequency in iNOS-SW480 cells was much higher than that in parent SW480 cells and was reduced to the level of mutation frequency in the parent cells by treatment with an NO synthase (NOS) inhibitor. Immunocytochemistry showed generation of more 8-nitroguanosine in iNOS-SW480 cells than in SW480 cells without iNOS transfection. Authentic 8-nitroguanosine added exogenously to GFP-SeV-infected CV-1 cells increased the viral mutation frequency. Profiles of the GFP gene mutations induced by 8-nitroguanosine appeared to resemble those of mutations occurring in mouse lungs in vivo. A base substitution that was characteristic of both mutants (those induced by 8-nitroguanosine and those occurring in vivo) was a C-to-U transition. NO-dependent oxidative stress in iNOS-SW480 cells was also evident. Together, the results indicate unambiguously that NO has mutagenic potential for RNA viruses such as Sendai virus without affecting viral replication, possibly via 8-nitroguanosine formation and cellular oxidative stress.</AbstractText>
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Nitric oxide as an endogenous mutagen for Sendai virus without antiviral activity.

Nitric oxide as an endogenous mutagen for Sendai virus without antiviral activity.

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