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1917 avian influenza virus sequences suggest that the 1918 pandemic virus did not acquire its hemagglutinin directly from birds.

ABSTRACT: Wild waterfowl captured between 1915 and 1919 were tested for influenza A virus RNA. One bird, captured in 1917, was infected with a virus of the same hemagglutinin (HA) subtype as that of the 1918 pandemic virus. The 1917 HA is more closely related to that of modern avian viruses than it is to that of the pandemic virus, suggesting (i) that there was little drift in avian sequences over the past 85 years and (ii) that the 1918 pandemic virus did not acquire its HA directly from a bird.

SUBMITTER: Fanning TG

PROVIDER: S-EPMC136362 | biostudies-literature | 2002 Aug

REPOSITORIES: biostudies-literature

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1917 avian influenza virus sequences suggest that the 1918 pandemic virus did not acquire its hemagglutinin directly from birds.

Fanning Thomas G TG Slemons Richard D RD Reid Ann H AH Janczewski Thomas A TA Dean James J Taubenberger Jeffery K JK

Journal of virology 20020801 15

Wild waterfowl captured between 1915 and 1919 were tested for influenza A virus RNA. One bird, captured in 1917, was infected with a virus of the same hemagglutinin (HA) subtype as that of the 1918 pandemic virus. The 1917 HA is more closely related to that of modern avian viruses than it is to that of the pandemic virus, suggesting (i) that there was little drift in avian sequences over the past 85 years and (ii) that the 1918 pandemic virus did not acquire its HA directly from a bird. ...[more]

PMID: 12097598

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Project description:UnlabelledZoonotic avian influenza virus infections may lead to epidemics or pandemics. The 1918 pandemic influenza virus has an avian influenza virus-like genome, and its H1 hemagglutinin was identified as a key mammalian virulence factor. A chimeric 1918 virus expressing a contemporary avian H1 hemagglutinin, however, displayed murine pathogenicity indistinguishable from that of the 1918 virus. Here, isogenic chimeric avian influenza viruses were constructed on an avian influenza virus backbone, differing only by hemagglutinin subtype expressed. Viruses expressing the avian H1, H6, H7, H10, and H15 subtypes were pathogenic in mice and cytopathic in normal human bronchial epithelial cells, in contrast to H2-, H3-, H5-, H9-, H11-, H13-, H14-, and H16-expressing viruses. Mouse pathogenicity was associated with pulmonary macrophage and neutrophil recruitment. These data suggest that avian influenza virus hemagglutinins H1, H6, H7, H10, and H15 contain inherent mammalian virulence factors and likely share a key virulence property of the 1918 virus. Consequently, zoonotic infections with avian influenza viruses bearing one of these hemagglutinins may cause enhanced disease in mammals.ImportanceInfluenza viruses from birds can cause outbreaks in humans and may contribute to the development of pandemics. The 1918 pandemic influenza virus has an avian influenza virus-like genome, and its main surface protein, an H1 subtype hemagglutinin, was identified as a key mammalian virulence factor. In a previous study, a 1918 virus expressing an avian H1 gene was as virulent in mice as the reconstructed 1918 virus. Here, a set of avian influenza viruses was constructed, differing only by hemagglutinin subtype. Viruses with the avian H1, H6, H7, H10, and H15 subtypes caused severe disease in mice and damaged human lung cells. Consequently, infections with avian influenza viruses bearing one of these hemagglutinins may cause enhanced disease in mammals, and therefore surveillance for human infections with these subtypes may be important in controlling future outbreaks.

Project description:Highly pathogenic avian influenza H5 viruses have pandemic potential, cause significant economic losses and are of veterinary and public health concerns. This study aimed to investigate the distribution and diversity of hemagglutinin (HA) subtypes of avian influenza virus (AIV) in poultry and wild birds in Bangladesh. We conducted an avian influenza sero-surveillance in wild and domestic birds in wetlands of Chattogram and Sylhet in the winter seasons 2012-2014. We tested serum samples using a competitive enzyme-linked immunosorbent assay (c-ELISA), and randomly selected positive serum samples (170 of 942) were tested using hemagglutination inhibition (HI) to detect antibodies against the 16 different HA sero-subtypes. All AIV sero-subtypes except H7, H11, H14 and H15 were identified in the present study, with H5 and H9 dominating over other subtypes, regardless of the bird species. The diversity of HA sero-subtypes within groups ranged from 3 (in household chickens) to 10 (in migratory birds). The prevalence of the H5 sero-subtype was 76.3% (29/38) in nomadic ducks, 71.4% (5/7) in household chicken, 66.7% (24/36) in resident wild birds, 65.9% (27/41) in migratory birds and 61.7% (29/47) in household ducks. Moreover, the H9 sero-subtype was common in migratory birds (56%; 23/41), followed by 38.3% (18/47) in household ducks, 36.8% (14/38) in nomadic ducks, 30.6% (11/66) in resident wild birds and 28.5% (2/7) in household chickens. H1, H4 and H6 sero-subtypes were the most common sero-subtypes (80%; 8/10, 70%; 7/10 and 70%; 7/10, respectively) in migratory birds in 2012, H9 in resident wild birds (83.3%; 5/6) and H2 in nomadic ducks (73.9%; 17/23) in 2013, and the H5 sero-subtype in all types of birds (50% to 100%) in 2014. The present study demonstrates that a high diversity of HA subtypes circulated in diverse bird species in Bangladesh, and this broad range of AIV hosts may increase the probability of AIVs' reassortment and may enhance the emergence of novel AIV strains. A continued surveillance for AIV at targeted domestic-wild bird interfaces is recommended to understand the ecology and evolution of AIVs.

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1917 avian influenza virus sequences suggest that the 1918 pandemic virus did not acquire its hemagglutinin directly from birds.

Publications

1917 avian influenza virus sequences suggest that the 1918 pandemic virus did not acquire its hemagglutinin directly from birds.

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