Pathogenicity and transmissibility of bovine H5N1 influenza virus

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Abstract

Highly pathogenic H5N1 avian influenza (HPAI H5N1) viruses occasionally infect, but typically do not transmit, in mammals. In the spring of 2024, an unprecedented outbreak of HPAI H5N1 in bovine herds occurred in the USA, with virus spread within and between herds, infections in poultry and cats, and spillover into humans, collectively indicating an increased public health risk ^{1–
4}. Here we characterize an HPAI H5N1 virus isolated from infected cow milk in mice and ferrets. Like other HPAI H5N1 viruses, the bovine H5N1 virus spread systemically, including to the mammary glands of both species, however, this tropism was also observed for an older HPAI H5N1 virus isolate. Bovine HPAI H5N1 virus bound to sialic acids expressed in human upper airways and inefficiently transmitted to exposed ferrets (one of four exposed ferrets seroconverted without virus detection). Bovine HPAI H5N1 virus thus possesses features that may facilitate infection and transmission in mammals.

Abstract

HPAI H5N1 virus isolated from infected cow milk is characterized in mice and ferrets, was inefficiently transmitted in ferrets, and bound to sialic acids expressed in human upper airways, showing features that may facilitate infection in mammals.

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Most cited references 28

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Molecular basis for high virulence of Hong Kong H5N1 influenza A viruses.

M Hatta (2001)

In 1997, an H5N1 influenza A virus was transmitted from birds to humans in Hong Kong, killing 6 of the 18 people infected. When mice were infected with the human isolates, two virulence groups became apparent. Using reverse genetics, we showed that a mutation at position 627 in the PB2 protein influenced the outcome of infection in mice. Moreover, high cleavability of the hemagglutinin glycoprotein was an essential requirement for lethal infection.

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A single amino acid in the PB2 gene of influenza A virus is a determinant of host range.

E Subbarao, W. London, B R Murphy (1993)

The single gene reassortant virus that derives its PB2 gene from the avian influenza A/Mallard/NY/78 virus and remaining genes from the human influenza A/Los Angeles/2/87 virus exhibits a host range restriction (hr) phenotype characterized by efficient replication in avian tissue and failure to produce plaques in mammalian Madin-Darby canine kidney cells. The hr phenotype is associated with restriction of viral replication in the respiratory tract of squirrel monkeys and humans. To identify the genetic basis of the hr phenotype, we isolated four phenotypic hr mutant viruses that acquired the ability to replicate efficiently in mammalian tissue. Segregational analysis indicated that the loss of the hr phenotype was due to a mutation in the PB2 gene itself. The nucleotide sequences of the PB2 gene of each of the four hr mutants revealed that a single amino acid substitution at position 627 (Glu-->Lys) was responsible for the restoration of the ability of the PB2 single gene reassortant to replicate in Madin-Darby canine kidney cells. Interestingly, the amino acid at position 627 in every avian influenza A virus PB2 protein analyzed to date is glutamic acid, and in every human influenza A virus PB2 protein, it is lysine. Thus, the amino acid at residue 627 of PB2 is an important determinant of host range of influenza A viruses.

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The viral polymerase mediates adaptation of an avian influenza virus to a mammalian host.

G Gabriel, B Dauber, T Wolff … (2005)

Mammalian influenza viruses are descendants of avian strains that crossed the species barrier and underwent further adaptation. Since 1997 in southeast Asia, H5N1 highly pathogenic avian influenza viruses have been causing severe, even fatal disease in humans. Although no lineages of this subtype have been established until now, such repeated events may initiate a new pandemic. As a model of species transmission, we used the highly pathogenic avian influenza virus SC35 (H7N7), which is low-pathogenic for mice, and its lethal mouse-adapted descendant SC35M. Specific mutations in SC35M polymerase considerably increase its activity in mammalian cells, correlating with high virulence in mice. Some of these mutations are prevalent in chicken and mammalian isolates, especially in the highly pathogenic H5N1 viruses from southeast Asia. These activity-enhancing mutations of the viral polymerase complex demonstrate convergent evolution in nature and, therefore, may be a prerequisite for adaptation to a new host paving the way for new pandemic viruses.

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Author and article information

Contributors

Yoshihiro Kawaoka:

ORCID: http://orcid.org/0000-0001-5061-8296

yoshihiro.kawaoka@wisc.edu

Journal

Journal ID (nlm-ta): Nature

Journal ID (iso-abbrev): Nature

Title: Nature

Publisher: Nature Publishing Group UK (London )

ISSN (Print): 0028-0836

ISSN (Electronic): 1476-4687

Publication date (Electronic): 8 July 2024

Publication date PMC-release: 8 July 2024

Publication date (Print): 2024

Volume: 633

Issue: 8029

Pages: 426-432

Affiliations

[1 ]Influenza Research Institute, Department of Pathobiological Sciences, University of Wisconsin-Madison, ( https://ror.org/01y2jtd41) Madison, WI USA

[2 ]Heritage Vet Partners, Johnson, KS USA

[3 ]Department of Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, ( https://ror.org/04rvw0k47) Shizuoka, Japan

[4 ]Texas A&M Veterinary Medical Diagnostic Laboratory, Canyon, TX USA

[5 ]GRID grid.264756.4, ISNI 0000 0004 4687 2082, Texas A&M Veterinary Medical Diagnostic Laboratory, ; College Station, TX USA

[6 ]Wisconsin Veterinary Diagnostic Laboratory, University of Wisconsin-Madison, ( https://ror.org/01y2jtd41) Madison, WI USA

[7 ]GRID grid.26999.3d, ISNI 0000 0001 2151 536X, Department of Virology, Institute of Medical Science, , University of Tokyo, ; Tokyo, Japan

[8 ]The University of Tokyo Pandemic Preparedness, Infection and Advanced Research Center (UTOPIA), University of Tokyo, ( https://ror.org/057zh3y96) Tokyo, Japan

[9 ]The Research Center for Global Viral Diseases, National Center for Global Health and Medicine Research Institute, ( https://ror.org/00r9w3j27) Tokyo, Japan

Author information

Peter J. Halfmann http://orcid.org/0000-0002-1648-1625

Alexis Thompson http://orcid.org/0000-0003-4405-5313

Kiril M. Dimitrov http://orcid.org/0000-0002-5525-4492

Yoshihiro Kawaoka http://orcid.org/0000-0001-5061-8296

Article

Publisher ID: 7766

DOI: 10.1038/s41586-024-07766-6

PMC ID: 11390473

PubMed ID: 38977017

SO-VID: 8c95ce09-6419-4d1f-93bb-2114cc09a1de

License:

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

History

Date received : 1 June 2024

Date accepted : 28 June 2024

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ScienceOpen disciplines: Uncategorized

Keywords: influenza virus,viral pathogenesis,viral transmission

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ScienceOpen disciplines: Uncategorized

Keywords: influenza virus, viral pathogenesis, viral transmission

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Pathogenicity and transmissibility of bovine H5N1 influenza virus

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IET: COVID-19 related research

Most cited references 28

Molecular basis for high virulence of Hong Kong H5N1 influenza A viruses.

A single amino acid in the PB2 gene of influenza A virus is a determinant of host range.

The viral polymerase mediates adaptation of an avian influenza virus to a mammalian host.

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