Highly Pathogenic Avian Influenza A(H5N1) Clade 2.3.4.4b Virus in Domestic Cat, France, 2022

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Abstract

We detected highly pathogenic avian influenza A(H5N1) clade 2.3.4.4b virus in a domestic cat that lived near a duck farm infected by a closely related virus in France during December 2022. Enhanced surveillance of symptomatic domestic carnivores in contact with infected birds is recommended to prevent further spread to mammals and humans.

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A single N66S mutation in the PB1-F2 protein of influenza A virus increases virulence by inhibiting the early interferon response in vivo.

Jennifer Tisoncik, M Katze, Elizabeth Rosenzweig … (2010)

The PB1-F2 protein of influenza A virus can contribute to viral pathogenesis of influenza virus strains. Of note, an N66S amino acid mutation in PB1-F2 has been shown to increase the pathogenesis associated with H5N1 Hong Kong/1997 and H1N1 Brevig Mission/1918 influenza viruses. To identify the mechanism of enhanced immunopathology, we evaluated the host response to two isogenic viruses that differ by a single amino acid at position 66 of the PB1-F2 protein. Various components of the adaptive immune response were ruled out as factors contributing to pathogenesis through knockout mouse studies. Transcriptional profiling of lungs from PB1-F2 66S-infected mice revealed an early delay in innate immune responses. In particular, enhanced activation of type I interferon (IFN) pathway genes, including IFN-β, RIG-I, and numerous interferon-inducible genes, was not observed until day 3 postinfection. The N66S mutant virus caused increased cellularity in the lungs, as a result of monocyte and neutrophil infiltration. Furthermore, numerous cytokines and chemokines related to monocyte and neutrophil migration and maturation were upregulated. The cellular infiltration and increased cytokine expression corresponded to increased PB1-F2 66S titer. These data suggest that PB1-F2 N66S may contribute to the delay of innate immune responses, allowing for unchecked viral growth and ultimately severe immunopathology observed in the lungs.

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Highly pathogenic avian influenza A(H5N1) virus infection in farmed minks, Spain, October 2022

Montserrat Agüero, Isabella Monne, Azucena Sánchez … (2023)

In October 2022, an outbreak in Europe of highly pathogenic avian influenza (HPAI) A(H5N1) in intensively farmed minks occurred in northwest Spain. A single mink farm hosting more than 50,000 minks was involved. The identified viruses belong to clade 2.3.4.4b, which is responsible of the ongoing epizootic in Europe. An uncommon mutation (T271A) in the PB2 gene with potential public health implications was found. Our investigations indicate onward mink transmission of the virus may have occurred in the affected farm.

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Adaptive mutations in the H5N1 polymerase complex.

Gülsah Gabriel, Volker Czudai, Hans Dieter Klenk (2013)

Adaptation of the viral polymerase to host factors plays an important role in interspecies transmission of H5N1 viruses. Several adaptive mutations have been identified that, in general, determine not only host range, but also pathogenicity and transmissibility of the virus. The available evidence indicates that most of these mutations are found in the PB2 subunit of the polymerase. Particularly prominent mutations are located in the C-terminal domain of PB2 involving the amino acid exchanges E627K and D701N. Both mutations, that are also responsible for the adaptation of other avian viruses to mammalian hosts, have been described in human H5N1 isolates. In animal models, it could be demonstrated that they enhance pathogenicity in mice and induce contact transmission in guinea pigs. Mutation E627K has also been identified as a determinant of air-borne H5N1 transmission in ferrets. We are only beginning to understand the underlying mechanisms at the molecular level. Thus, mutation D701N promotes importin-α mediated nuclear transport in mammalian cells. Mutation E627K also enhances the replication rate in an importin-α dependent fashion in mammalian cells, yet without affecting nuclear entry of PB2. Numerous other adaptive mutations, some of which compensate for the lack of PB2 E627K, have been observed in PB2 as well as in the polymerase subunit PB1, the nucleoprotein NP, and the nuclear export protein NEP (NS2). Copyright © 2013 Elsevier B.V. All rights reserved.

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Author and article information

Journal

Journal ID (nlm-ta): Emerg Infect Dis

Journal ID (iso-abbrev): Emerg Infect Dis

Journal ID (publisher-id): EID

Title: Emerging Infectious Diseases

Publisher: Centers for Disease Control and Prevention

ISSN (Print): 1080-6040

ISSN (Electronic): 1080-6059

Publication date (Print): August 2023

Volume: 29

Issue: 8

Pages: 1696-1698

Affiliations

[1]ANSES, Ploufragan, France (F.-X. Briand, F. Souchaud, I. Pierre, V. Beven, E. Hirchaud, N. Eterradossi, A. Schmitz, E. Niqueux, B. Grasland);

[2]Clinique Vétérinaire des Deux Rivières, Mauléon, France (F. Hérault);

[3]Clinique Vétérinaire Filiavet, Bressuire, France (R. Planel);

[4]Resalab Ouest site de Labovet Analyse, Les Herbiers, France (A. Rigaudeau);

[5]Santé publique France, Saint-Maurice, France (S. Bernard-Stoecklin);

[6]Université Paris Cité Institut Pasteur National Reference Center, Paris, France (S. Van der Werf);

[7]National Reference Center for Respiratory Viruses, Lyon, France (B. Lina);

[8]Université de Lyon, Lyon (B. Lina);

[9]French Ministry of Food and Agriculture, Paris (G. Gerbier)

Author notes

Address for correspondence: François-Xavier Briand, Anses, Laboratoire de Ploufragan-Plouzané-Niort, Zoopôle-Les Croix, BP 53, 22440 Ploufragan, France; email: francois-xavier.briand@ 123456anses.fr

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Publisher ID: 23-0188

DOI: 10.3201/eid2908.230188

PMC ID: 10370847

PubMed ID: 37379514

SO-VID: e945e7a7-bb30-40c7-a850-12bd3d00b427

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Emerging Infectious Diseases is a publication of the U.S. Government. This publication is in the public domain and is therefore without copyright. All text from this work may be reprinted freely. Use of these materials should be properly cited.

Highly Pathogenic Avian Influenza A(H5N1) Clade 2.3.4.4b Virus in Domestic Cat, France, 2022

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Most cited references 8

A single N66S mutation in the PB1-F2 protein of influenza A virus increases virulence by inhibiting the early interferon response in vivo.

Highly pathogenic avian influenza A(H5N1) virus infection in farmed minks, Spain, October 2022

Adaptive mutations in the H5N1 polymerase complex.

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