Abstract
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 α2,3 versus α2,6, 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 α2,3 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 α2,3 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.
Highlights
Influenza A viruses are important pathogens that present a significant threat to public health, causing an extensive economic burden for avian influenza virus (AIV) infection of poultry
We determined if low pathogenic H5N1, H5N2 and H5N3 AIV isolates of chicken or wild bird origin could infect and replicate in fully differentiated, normal human bronchial epithelial (NHBE) cells. We show that these viruses infect, replicate, and are released from NHBE cells independent of detectable sia a2,3 or a2,6 moieties present on the cell surface, and show that low pathogenic AIV (LPAI) H5N1, H5N2 and H5N3 viruses induce higher inducible protein of 10 kD (IP-10) and RANTES responses early during infection compared to human H3N2 infection indicating differential chemokine expression patterns that may contribute to the unique aspects of disease pathogenesis between avian and human influenza virus infection
NHBE cells express a2,6 and a2,3 sialic acid receptors To determine if the propensity of AIVs to infect NHBE cells was related to sia a2,3 tropism, the cells were stained with sia-specific lectins
Summary
Influenza A viruses are important pathogens that present a significant threat to public health, causing an extensive economic burden for avian influenza virus (AIV) infection of poultry. Influenza viruses are segmented, enveloped, negativestrand RNA viruses belonging to the Orthomyxoviridae family. It remains unclear the precise features that contributed to the high rate of mortality due to infection with the 1918 influenza virus, but it has been shown that a single mutation in the PB1-F2 genome of 1918 influenza A viruses ( recognized for highly pathogenic H5N1 avian influenza) contributed to increased virulence [3,4,5]. Since 2003, there has been an increased incidence of highly pathogenic avian influenza (HPAI) virus outbreaks in poultry, and HPAI H5N1 has crossed species barriers to infect .500 humans resulting in nearly a 60% fatality rate (.300 deaths) as of April 2011 [6]
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