OmniVira

Literature detail

Pigs are highly susceptible to but do not transmit mink-derived highly pathogenic avian influenza virus H5N1 clade 2.3.4.4b.

Taeyong Kwon1 Jessie D Trujillo1 Mariano Carossino2 Eu Lim Lyoo1 Chester D McDowell1 Konner Cool1 Franco S Matias-Ferreyra1 Trushar Jeevan3 Igor Morozov1 Natasha N Gaudreault1 Udeni B R Balasuriya2 Richard J Webby3 Nikolaus Osterrieder1 Juergen A Richt1
Affiliations 3 institutions
  1. Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA.
  2. Louisiana Animal Disease Diagnostic Laboratory and Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, USA.
  3. Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, USA.
PMID 38712345 2024 Emerg Microbes Infect eng ppublish
PubMed DOI Browse context

Article

Publication summary

<b>ABSTRACT</b>Rapid evolution of highly pathogenic avian influenza viruses (HPAIVs) is driven by antigenic drift but also by reassortment, which might result in robust replication in and transmission to mammals. Recently, spillover of clade 2.3.4.4b HPAIV to mammals including humans, and their transmission between mammalian species has been reported. This study aimed to evaluate the pathogenicity and transmissibility of a mink-derived clade 2.3.4.4b H5N1 HPAIV isolate from Spain in pigs. Experimental infection caused interstitial pneumonia with necrotizing bronchiolitis with high titers of virus present in the lower respiratory tract and 100% seroconversion. Infected pigs shed limited amount of virus, and importantly, there was no transmission to contact pigs. Notably, critical mammalian-like adaptations such as PB2-E627 K and HA-Q222L emerged at low frequencies in principal-infected pigs. It is concluded that pigs are highly susceptible to infection with the mink-derived clade 2.3.4.4b H5N1 HPAIV and provide a favorable environment for HPAIV to acquire mammalian-like adaptations.

clade 2.3.4.4b H5N1 highly pathogenic avian influenza virus mammalian-like adaptations, mink isolate, transmission Pigs Influenza A Virus, H5N1 Subtype Mink Orthomyxoviridae Infections Swine Diseases Animals Spain Swine Viral Proteins Virus Shedding

Structured evidence records

Evidence records

3 total
Host Range Experiment 1 records
Host Range Experiment Extraction confidence 1.00
Key finding

Experimental infection showed that pigs were highly susceptible to the mink-derived clade 2.3.4.4b H5N1 HPAIV, showing strong replication and seroconversion but no onward transmission to contact pigs.

Virus
IAV H5N1
Location
Not specified
Supporting text

This study aimed to evaluate the pathogenicity and transmissibility of a mink-derived clade 2.3.4.4b H5N1 HPAIV isolate from Spain in pigs. Experimental infection caused interstitial pneumonia with necrotizing bronchiolitis with high titers of virus present in the lower respiratory tract and 100% seroconversion. Infected pigs shed limited amount of virus, and importantly, there was no transmission to contact pigs.

Method
experimental infection; transmission study
Sample type
lower respiratory tract
Experimental system
in vivo animal experiment
Molecular Adaptation 1 records
Molecular Adaptation Extraction confidence 0.95
Key finding

The mink-derived clade 2.3.4.4b H5N1 virus showed emergence of mammalian-like mutations PB2-E627K and HA-Q222L during infection of pigs.

Virus
IAV H5N1
Host
Not specified
Location
Not specified
Supporting text

Notably, critical mammalian-like adaptations such as PB2-E627K and HA-Q222L emerged at low frequencies in principal-infected pigs.

Genes or proteins
PB2; HA
Mutations
PB2-E627K; HA-Q222L
Mechanism types
polymerase_activity; receptor_binding
Serological Evidence 1 records
Serological Evidence Extraction confidence 0.90
Key finding

Pigs experimentally infected with mink-derived H5N1 clade 2.3.4.4b developed antibodies with 100% seroconversion, demonstrating serological evidence of infection.

Virus
IAV H5N1
Host
Sus scrofa
Location
Not specified
Supporting text

Experimental infection caused interstitial pneumonia with necrotizing bronchiolitis with high titers of virus present in the lower respiratory tract and 100% seroconversion.

Sample type
serum