Avian Influenza Viruses Infect Primary Human Bronchial Epithelial Cells Unconstrained by Sialic Acid α2,3 Residues

被引:44
|
作者
Oshansky, Christine M. [1 ]
Pickens, Jennifer A. [1 ]
Bradley, Konrad C. [2 ]
Jones, Les P. [1 ]
Saavedra-Ebner, Geraldine M. [1 ]
Barber, James P. [1 ]
Crabtree, Jackelyn M. [1 ]
Steinhauer, David A. [2 ]
Tompkins, S. Mark [1 ]
Tripp, Ralph A. [1 ]
机构
[1] Univ Georgia, Coll Vet Med, Dept Infect Dis, Athens, GA 30602 USA
[2] Emory Univ, Sch Med, Dept Microbiol & Immunol, Atlanta, GA 30322 USA
来源
PLOS ONE | 2011年 / 6卷 / 06期
关键词
RECEPTOR-BINDING SPECIFICITY; HUMAN AIRWAY EPITHELIUM; I INTERFERON RESPONSE; A H5N1 VIRUSES; MAACKIA-AMURENSIS; CYTOKINE RESPONSES; GENE-EXPRESSION; HUMAN ALVEOLAR; HOST-RANGE; H1N1;
D O I
10.1371/journal.pone.0021183
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Avian influenza viruses (AIV) are an important emerging threat to public health. It is thought that sialic acid (sia) receptors are barriers in cross-species transmission where the binding preferences of AIV and human influenza viruses are sias alpha 2,3 versus alpha 2,6, respectively. In this study, we show that a normal fully differentiated, primary human bronchial epithelial cell model is readily infected by low pathogenic H5N1, H5N2 and H5N3 AIV, which primarily bind to sia alpha 2,3 moieties, and replicate in these cells independent of specific sias on the cell surface. NHBE cells treated with neuraminidase prior to infection are infected by AIV despite removal of sia alpha 2,3 moieties. Following AIV infection, higher levels of IP-10 and RANTES are secreted compared to human influenza virus infection, indicating differential chemokine expression patterns, a feature that may contribute to differences in disease pathogenesis between avian and human influenza virus infections in humans.
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页数:12
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