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Titolo:
Viral mutation accelerated by nitric oxide production during infection in vivo
Autore:
Akaike, T; Fujii, S; Kato, A; Yoshitake, J; Miyamoto, Y; Sawa, T; Okamoto, S; Suga, M; Asakawa, M; Nagai, Y; Maeda, H;
Indirizzi:
Kumamoto Univ, Sch Med, Dept Microbiol, Kumamoto 8600811, Japan Kumamoto Univ Kumamoto Japan 8600811 Microbiol, Kumamoto 8600811, Japan Kumamoto Univ, Sch Med, Dept Med 1, Kumamoto 8600811, Japan Kumamoto UnivKumamoto Japan 8600811 Dept Med 1, Kumamoto 8600811, Japan Univ Tokyo, Inst Ind Sci, Dept Viral Infect, Tokyo 1080071, Japan Univ Tokyo Tokyo Japan 1080071 , Dept Viral Infect, Tokyo 1080071, Japan DNAVEC Res Inst, Tsukuba, Ibaraki, Japan DNAVEC Res Inst Tsukuba Ibaraki Japan Res Inst, Tsukuba, Ibaraki, Japan
Titolo Testata:
FASEB JOURNAL
fascicolo: 10, volume: 14, anno: 2000,
pagine: 1447 - 1454
SICI:
0892-6638(200007)14:10<1447:VMABNO>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
SENDAI VIRUS; VESICULAR STOMATITIS; OXYGEN RADICALS; PEROXYNITRITE; MICE; PATHOGENESIS; MUTAGENESIS; SUPEROXIDE; CARCINOGENESIS; FREQUENCIES;
Keywords:
NO; peroxynitrite; oxidative stress;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Akaike, T Kumamoto Univ, Sch Med, Dept Microbiol, Kumamoto 8600811, Japan Kumamoto Univ Kumamoto Japan 8600811 , Kumamoto 8600811, Japan
Citazione:
T. Akaike et al., "Viral mutation accelerated by nitric oxide production during infection in vivo", FASEB J, 14(10), 2000, pp. 1447-1454

Abstract

Nitric oxide (NO), superoxide (O-2(-)), and their reaction product peroxynitrite (ONOO-) are generated in excess during a host's response against viral infection, and contribute to viral pathogenesis by promoting oxidative stress and tissue injury. Here we demonstrate that NO and peroxynitrite greatly accelerates the mutation of Sendai virus (SeV), a nonsegmented negative-strand RNA virus, by using green fluorescent protein (GFP) inserted into and expressed by a recombinant SeV (GFP-SeV) as an indicator for mutation. GFP-SeV mutation frequencies were much higher in the wild-type mice than in those lacking inducible NO synthase, suggesting that mutation of the virus in vivo is NO dependent. High levels of NO and NO-mediated oxidative stresswere induced by GFP-SeV infection in the lung of the wild-type mice, but not in the iNOS-deficient mice, as evidenced by electron spin resonance spectroscopy and immunohistochemical analysis for nitrotyrosine formation as well as histopathological examination. Furthermore, peroxynitrite, an NO-derived reactive nitrogen intermediate, enhanced viral mutation in vitro. Theseresults indicate that the oxidative stress induced by NO produced during the natural course of viral infection increases mutation, expands the quasispecies spectrum, and facilitates evolution of RNA viruses.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/20 alle ore 15:12:50