Evolution and molecular epidemiology of H9N2 influenza A viruses from Quail in southern China, 2000 to 2005

被引:148
作者
Xu, K. M.
Li, K. S.
Smith, G. J. D.
Li, J. W.
Tai, H.
Zhang, J. X.
Webster, R. G.
Peiris, J. S. M.
Chen, H.
Guan, Y.
机构
[1] Univ Hong Kong, Dept Microbiol, State Key Lab Emerging Infect Dis, Li Ka Sing Fac Med, Hong Kong, Peoples R China
[2] Shantou Univ, Coll Med, Joint Influenza Res Ctr, SUMC & HKU, Shantou 515031, Guangdong, Peoples R China
[3] St Jude Childrens Res Hosp, Div Virol, Dept Infect Dis, Memphis, TN 38105 USA
关键词
D O I
10.1128/JVI.02316-06
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
H9N2 influenza viruses have become established and maintain long-term endemicity in terrestrial poultry in Asian countries. Occasionally these viruses transmit to other mammals, including humans. Increasing epidemiological and laboratory findings suggest that quail may be an important host, as they are susceptible to different subtypes of influenza viruses. To better understand the role of quail in influenza virus ecology and evolution, H9N2 viruses isolated from quail during 2000 to 2005 were antigenically and genetically characterized. Our results showed that H9N2 viruses are prevalent year-round in southern China and replicate mainly asymptomatically in the respiratory tract of quail. Genetic analysis revealed that both the G1-like and Ck/Bei-like H9N2 lineages were cocirculating in quail since 2000. Phylogenetic analyses demonstrated that most of the isolates tested were double- or multiple-reassortant variants, with four G1-like and 16 Ck/Bei-like genotypes recognized. A novel genotype of GI-like virus became predominant in quail since 2003, while multiple Ck/Bei-like genotypes were introduced into quail, wherein they incorporated G1-like gene segments, but none of them became established in this host. Those Ck/Bei-like reassortants generated in quail have then been introduced into other poultry. These complex interactions form a two-way transmission system between quail and other types of poultry. The present study provides evidence that H9N2 and H5N1 subtype viruses have also exchanged gene segments to generate currently circulating reassortants of both subtypes that have pandemic potential. Continuing influenza virus surveillance in poultry is critical to understanding the genesis and emergence of potentially pandemic strains in this region.
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页码:2635 / 2645
页数:11
相关论文
共 40 条
[31]   Human infection with influenza H9N2 [J].
Peiris, M ;
Yuen, KY ;
Leung, CW ;
Chan, KH ;
Ip, PLS ;
Lai, RWM ;
Orr, WK ;
Shortridge, KF .
LANCET, 1999, 354 (9182) :916-917
[32]   Lethal H5N1 influenza viruses escape host anti-viral cytokine responses [J].
Seo, SH ;
Hoffmann, E ;
Webster, RG .
NATURE MEDICINE, 2002, 8 (09) :950-954
[33]  
Shortridge K F, 1992, Semin Respir Infect, V7, P11
[34]  
SHORTRIDGE KF, 1982, LANCET, V2, P812
[35]   Evolution and adaptation of H5N1 influenza virus in avian and human hosts in Indonesia and Vietnam [J].
Smith, G. J. D. ;
Naipospos, T. S. P. ;
Nguyen, T. D. ;
de Jong, M. D. ;
Vijaykrishna, D. ;
Usman, T. B. ;
Hassan, S. S. ;
Nguyen, T. V. ;
Dao, T. V. ;
Bui, N. A. ;
Leung, Y. H. C. ;
Cheung, C. L. ;
Rayner, J. M. ;
Zhang, J. X. ;
Zhang, L. J. ;
Poon, L. L. M. ;
Li, K. S. ;
Nguyen, V. C. ;
Hien, T. T. ;
Farrar, J. ;
Webster, R. G. ;
Chen, H. ;
Peiris, J. S. M. ;
Guan, Y. .
VIROLOGY, 2006, 350 (02) :258-268
[36]  
Sokal R.R., 1958, University of Kansas science Bulletin, V38, P1409
[37]   Role of hemagglutinin cleavage for the pathogenicity of influenza virus [J].
Steinhauer, DA .
VIROLOGY, 1999, 258 (01) :1-20
[38]   EVOLUTION AND ECOLOGY OF INFLUENZA-A VIRUSES [J].
WEBSTER, RG ;
BEAN, WJ ;
GORMAN, OT ;
CHAMBERS, TM ;
KAWAOKA, Y .
MICROBIOLOGICAL REVIEWS, 1992, 56 (01) :152-179
[39]   Characterization of H5N1 influenza viruses that continue to circulate in geese in southeastern China [J].
Webster, RG ;
Guan, Y ;
Peiris, M ;
Walker, D ;
Krauss, S ;
Zhou, NN ;
Govorkova, EA ;
Ellis, TM ;
Dyrting, KC ;
Sit, T ;
Perez, DR ;
Shortridge, KF .
JOURNAL OF VIROLOGY, 2002, 76 (01) :118-126
[40]  
XU X, 2004, MICROBES INFECT, V10, P919