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Titolo:
Biological heterogeneity, including systemic replication in mice, of H5N1 influenza A virus isolates from humans in Hong Kong
Autore:
Gao, P; Watanabe, S; Ito, T; Goto, H; Wells, K; McGregor, M; Cooley, AJ; Kawaoka, Y;
Indirizzi:
Univ Wisconsin, Sch Vet Med, Dept Pathobiol Sci, Madison, WI 53706 USA Univ Wisconsin Madison WI USA 53706 Pathobiol Sci, Madison, WI 53706 USA HokkaidoHokkaidorad Sch Vet Med, Dept Dis Control, Microbiol Lab, Sapporo,Hokkaido Univ Sapporo Hokkaido Japan 0600818 rol, Microbiol Lab, Sapporo, Tottori Univ, Fac Agr, Dept Vet Publ Hlth, Tottori 6800945, Japan Tottori Univ Tottori Japan 6800945 Vet Publ Hlth, Tottori 6800945, Japan
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 4, volume: 73, anno: 1999,
pagine: 3184 - 3189
SICI:
0022-538X(199904)73:4<3184:BHISRI>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
SINGLE AMINO-ACID; A VIRUS; HEMAGGLUTININ; CLEAVAGE; FURIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Kawaoka, Y Univ Wisconsin, Sch Vet Med, Dept Pathobiol Sci, 2015 Linden DrW, Madison, Univ Wisconsin 2015 Linden Dr W Madison WI USA 53706 , Madison,
Citazione:
P. Gao et al., "Biological heterogeneity, including systemic replication in mice, of H5N1 influenza A virus isolates from humans in Hong Kong", J VIROLOGY, 73(4), 1999, pp. 3184-3189

Abstract

An H5N1 avian influenza A virus was transmitted to humans in Hong Kong in 1997. Although the virus causes systemic infection and is highly lethal in chickens because of the susceptibility of the hemagglutinin to furin and PCB proteases, it is not known whether it also causes systemic infection in humans. The clinical outcomes of infection in Hong Kong residents ranged widely, from mild respiratory disease to multiple organ failure leading to death. Therefore, to understand the pathogenesis of influenza due to these H5N1 isolates, we investigated their virulence in mice. The results identifiedtwo distinct groups of viruses: group I, for which the dose lethal for 50%of mice (MLD50) was between 0.3 and 11 PFU, and group 2, for which the MLD50 was more than 10(3) PFU. One day after intranasal inoculation of mice with 100 PFU of group 1 viruses, the virus titer in lungs was 10(7) PFU/g or 3 log units higher than that for group 2 viruses. Both types of viruses hadreplicated to high titers (>10(6) PFU/g) in the lungs by day 3 and maintained these titers through day 6. More importantly, only the group I viruses caused systemic infection, replicating in nonrespiratory organs, including the brain, Immunohistochemical analysis demonstrated the replication of a group I virus in brain neurons and glial cells and in cardiac myofibers, Phylogenetic analysis of all viral genes showed that both groups of Hong Kong H5N1 viruses had formed a lineage distinct from those of other viruses and that genetic reassortment between H5N1 and H1 or H3 human viruses had not occurred. Since mice and humans harbor both the furin and the PC6 proteases,we suggest that the virulence mechanism responsible for the lethality of influenza viruses in birds also operates in mammalian hosts. The failure of some H5N1 viruses to produce systemic infection in our model indicates thatmultiple, still-to-be-identified, factors contribute to the severity of H5N1 infection in mammals. In addition, the ability of these viruses to produce systemic infection in mice and the clear differences in pathogenicity among the isolates studied here indicate that this system provides a useful model for studying the pathogenesis of avian influenza virus infection in mammals.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 07:15:35