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Antigenic evolution of H3N2 influenza A viruses in swine in the United States from 2012 to 2016.

Thu, 09/20/2018 - 07:00
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Antigenic evolution of H3N2 influenza A viruses in swine in the United States from 2012 to 2016.

Influenza Other Respir Viruses. 2018 Sep 14;:

Authors: Bolton MJ, Abente EJ, Venkatesh D, Stratton JA, Zeller M, Anderson TK, Lewis NS, Vincent AL

Abstract
BACKGROUND: Six amino acid positions (145, 155, 156, 158, 159 and 189, referred to as the antigenic motif; H3 numbering) in the globular head region of hemagglutinin (HA1 domain) play an important role in defining the antigenic phenotype of swine Clade IV (C-IV) H3N2 IAV, containing an H3 from a late 1990s human-to-swine introduction. We hypothesized that antigenicity of a swine C-IV H3 virus could be inferred based upon the antigenic motif if it matched a previously characterized antigen with the same motif. An increasing number of C-IV H3 genes encoding antigenic motifs that had not been previously characterized were observed in the U.S. pig population between 2012-2016.
OBJECTIVES: A broad panel of contemporary H3 viruses with uncharacterized antigenic motifs were selected across multiple clades within C-IV to assess the impact of HA1 genetic diversity on the antigenic phenotype.
METHODS: Hemagglutination inhibition (HI) assays were performed with isolates selected based on antigenic motif, tested against a panel of swine anti-sera, and visualized by antigenic cartography.
RESULTS: A previously uncharacterized motif with low but sustained circulation in the swine population demonstrated a distinct phenotype from those previously characterized. Antigenic variation increased for viruses with similar antigenic motifs, likely due to amino acid substitutions outside the motif.
CONCLUSIONS: Although antigenic motifs were largely associated with antigenic distances, substantial diversity among co-circulating viruses poses a significant challenge for effective vaccine development. Continued surveillance and antigenic characterization of circulating strains is critical for improving vaccine efforts to control C-IV H3 IAV in U.S. swine. This article is protected by copyright. All rights reserved.

PMID: 30216671 [PubMed - as supplied by publisher]

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Substitution of D701N in the PB2 protein could enhance the viral replication and pathogenicity of Eurasian avian-like H1N1 swine influenza viruses.

Thu, 09/20/2018 - 07:00
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Substitution of D701N in the PB2 protein could enhance the viral replication and pathogenicity of Eurasian avian-like H1N1 swine influenza viruses.

Emerg Microbes Infect. 2018 May 02;7(1):75

Authors: Liu S, Zhu W, Feng Z, Gao R, Guo J, Li X, Liu J, Wang D, Shu Y

Abstract
Eurasian avian-like H1N1 (EA H1N1) swine influenza viruses (SIVs) have become predominant in pig populations in China and have recently been reported to have the most potential to raise the next pandemic in humans. The mutation D701N in the PB2 protein, which accounts for 31% of H1N1 SIVs, has previously been shown to contribute to the adaptation of the highly pathogenic H5N1 or H7N7 avian influenza viruses in mammals. However, little is known of the effects of this substitution on the EA H1N1 viruses. Herein, we investigated the contributions of 701N in the PB2 protein to an EA H1N1 SIV (A/Hunan/42443/2015(H1N1), HuN EA-H1N1), which had 701D in the PB2 protein. Our results found that viral polymerase activity, viral replication, and pathogenicity in mice were indeed enhanced due to the introduction of 701N into the PB2 protein, and the increased viral growth was partly mediated by the host factor importin-α7. Thus, substantial attention should be paid to the D701N mutation in pig populations.

PMID: 29717109 [PubMed - indexed for MEDLINE]

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