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Titolo:
Plasminogen-binding activity of neuraminidase determines the pathogenicityof influenza A virus
Autore:
Goto, H; Wells, K; Takada, A; Kawaoka, Y;
Indirizzi:
Univ Wisconsin, Dept Pathobiol Sci, Sch Vet Med, Madison, WI 53706 USA Univ Wisconsin Madison WI USA 53706 i, Sch Vet Med, Madison, WI 53706 USA Univ Tokyo, Inst Med Sci, Tokyo 1088639, Japan Univ Tokyo Tokyo Japan 1088639 Tokyo, Inst Med Sci, Tokyo 1088639, Japan Hokkaido Univ, Grad Sch Vet Med, Dept Dis Control, Microbiol Lab, Sapporo,Hokkaido 0600818, Japan Hokkaido Univ Sapporo Hokkaido Japan 0600818 poro,Hokkaido 0600818, Japan
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 19, volume: 75, anno: 2001,
pagine: 9297 - 9301
SICI:
0022-538X(200110)75:19<9297:PAONDT>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
A VIRUS; HEMAGGLUTININ; ACTIVATION; CLEAVAGE; VIRULENCE; GENE; PLASMIN(OGEN); MECHANISM; FURIN; CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Kawaoka, Y Univ Wisconsin, Dept Pathobiol Sci, Sch Vet Med, 2015 Linden Dr, Madison, WI 53706 USA Univ Wisconsin 2015 Linden Dr Madison WI USA 53706 WI 53706 USA
Citazione:
H. Goto et al., "Plasminogen-binding activity of neuraminidase determines the pathogenicityof influenza A virus", J VIROLOGY, 75(19), 2001, pp. 9297-9301

Abstract

When expressed in vitro, the neuraminidase (NA) of A/WSN/33 (WSN) virus binds and sequesters plasminogen on the cell surface, leading to enhanced cleavage of the viral hemagglutinin. To obtain direct evidence that the plasminogen-binding activity of the NA enhances the pathogenicity of WSN virus, we generated mutant viruses whose NAs lacked plasminogen-binding activity because of a mutation at the C terminus, from Lys to Arg or Leu. In the presence of trypsin, these mutant viruses replicated similarly to wild-type virus in cell culture. By contrast, in the presence of plasminogen, the mutant viruses failed to undergo multiple cycles of replication while the wild-type virus grew normally. The mutant viruses showed attenuated growth in mice and failed to grow at all in the brain. Furthermore, another mutant WSN virus, possessing an NA with a glycosylation site at position 130 (146 in N2 numbering), leading to the loss of neurovirulence, failed to grow in cell culture in the presence of plasminogen. We conclude that the plasminogen-binding activity of the WSN NA determines its pathogenicity in mice.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 06:57:10