Dataset Information

Phylogenetic analysis of low pathogenicity H5N1 and H7N3 influenza A virus isolates recovered from sentinel, free flying, wild mallards at one study site during 2006.

ABSTRACT: From August 2 to October 11, 2006, clusters of low pathogenicity (LP) North American lineage H5N1 and H7N3 avian influenza A viruses (AIV), and other subtypes, were recovered from free-flying, resident, wild mallards used as sentinels at one site. The antigenic subtypes, pathogenicity potential, and Sanger sequencing of the isolates determined the H5N1 and H7N3 isolates were only recovered from samples collected on 8/2/2006 and 9/8/2006, respectively. However, subsequent efforts using next-generation sequencing (NGS) and additional Sanger sequencing found partial H7 segments in other HA-NA virus combinations on 8/2/2006, 9/8/2006 and 10/11/2006. It is well established that over larger geographic areas and years AIVs form transient genomic constellations; this sequential sampling data revealed that over a short period of time the dynamics of AIVs can be active and newer sequencing platforms increase recognition of mixed infections. Both findings provide further insight into the natural history of AIVs in natural reservoirs.

SUBMITTER: Dugan VG

PROVIDER: S-EPMC3157087 | biostudies-literature | 2011 Aug

REPOSITORIES: biostudies-literature

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Phylogenetic analysis of low pathogenicity H5N1 and H7N3 influenza A virus isolates recovered from sentinel, free flying, wild mallards at one study site during 2006.

Dugan Vivien G VG Dunham Eleca J EJ Jin Guozhong G Sheng Zong-Mei ZM Kaser Emilee E Nolting Jacqueline M JM Alexander H Lloyd HL Slemons Richard D RD Taubenberger Jeffery K JK

Virology 20110612 1

From August 2 to October 11, 2006, clusters of low pathogenicity (LP) North American lineage H5N1 and H7N3 avian influenza A viruses (AIV), and other subtypes, were recovered from free-flying, resident, wild mallards used as sentinels at one site. The antigenic subtypes, pathogenicity potential, and Sanger sequencing of the isolates determined the H5N1 and H7N3 isolates were only recovered from samples collected on 8/2/2006 and 9/8/2006, respectively. However, subsequent efforts using next-gener ...[more]

PMID: 21658737

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Project description:Outbreaks of highly pathogenic avian influenza (HPAI) virus subtype H7N3 have been occurring in commercial chickens in Mexico since its first introduction in 2012. In order to determine changes in virus pathogenicity and adaptation in avian species, three H7N3 HPAI viruses from 2012, 2015, and 2016 were evaluated in chickens and mallards. All three viruses caused high mortality in chickens when given at medium to high doses and replicated similarly. No mortality or clinical signs and similar infectivity were observed in mallards inoculated with the 2012 and 2016 viruses. However, the 2012 H7N3 HPAI virus replicated well in mallards and transmitted to contacts, whereas the 2016 virus replicated poorly and did not transmit to contacts, which indicates that the 2016 virus is less adapted to mallards. In vitro, the 2016 virus grew slower and to lower titers than did the 2012 virus in duck fibroblast cells. Full-genome sequencing showed 115 amino acid differences between the 2012 and the 2016 viruses, with some of these changes previously associated with changes in replication in avian species, including hemagglutinin (HA) A125T, nucleoprotein (NP) M105V, and NP S377N. In conclusion, as the Mexican H7N3 HPAI virus has passaged through large populations of chickens in a span of several years and has retained its high pathogenicity for chickens, it has decreased in fitness in mallards, which could limit the potential spread of this HPAI virus by waterfowl.IMPORTANCE Not much is known about changes in host adaptation of avian influenza (AI) viruses in birds after long-term circulation in chickens or other terrestrial poultry. Although the origin of AI viruses affecting poultry is wild aquatic birds, the role of these birds in further dispersal of poultry-adapted AI viruses is not clear. Previously, we showed that HPAI viruses isolated early from poultry outbreaks could still infect and transmit well in mallards. In this study, we demonstrate that the Mexican H7N3 HPAI virus after four years of circulation in chickens replicates poorly and does not transmit in mallards but remains highly pathogenic in chickens. This information on changes in host adaptation is important for understanding the epidemiology of AI viruses and the role that wild waterfowl may play in disseminating viruses adapted to terrestrial poultry.

Project description:BackgroundSince the first outbreak recorded in northern areas of Pakistan in early 2006, highly pathogenic avian influenza H5N1 viruses were isolated from commercial poultry and wild/domestic birds from different areas of Pakistan up to July 2008. Different isolates of H5N1 were sequenced to explore the genetic diversity of these viruses.ResultsPhylogenetic analysis revealed close clustering and highest sequence identity in all 8 genes to HPAI H5N1 isolates belonging to unified H5 clade 2.2, sub-lineage EMA-3 recovered from Afghanistan during the same time period. Two subgroups within Pakistani H5N1 viruses, from domestic and wild birds, were observed on the basis of their sequence homology and mutations. HPAI motif, preferred receptor specificity for α-(2, 3) linkages, potential N-linked glycosylation sites and an additional glycosylation site at the globular head of HA protein of four Pakistani H5N1 isolates. While, the amino acids associated with sensitivities to various antiviral drugs (Oseltamivir, Zanamivir, Amantadine) were found conserved for the Pakistani H5N1 isolates. Conspicuously, some important mutations observed at critical positions of antigenic sites (S141P, D155S, R162I & P181S) and at receptor binding pocket (A185T, R189K & S217P) of HA-1. A high sequence similarity between Pakistani HP H5N1 and LP H9N2 viruses was also observed. Avian like host specific markers with the exception of E627K in PB2, K356R in PA, V33I in NP, I28V in M2 and L107F in NS2 proteins were also observed.ConclusionsVarious point mutations in different genes of H5 viruses from Pakistan were observed during its circulation in the field. The outbreaks started in Khyber Pakhtoon Khawa (North West) province in 2006 and spread to the Southern regions over a period of time. Though migratory birds may have a role for this continued endemicity of clade 2.2 H5N1 viruses during 2006-2008 in Pakistan, the possibility of their transmission through legal or illegal poultry trade across the borders cannot be ignored.

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Dataset Information

Phylogenetic analysis of low pathogenicity H5N1 and H7N3 influenza A virus isolates recovered from sentinel, free flying, wild mallards at one study site during 2006.

Publications

Phylogenetic analysis of low pathogenicity H5N1 and H7N3 influenza A virus isolates recovered from sentinel, free flying, wild mallards at one study site during 2006.

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