Novel isoforms of influenza virus PA-X and PB1-F2 indicated by automatic annotation

Burnham, Andrew J.; Miller, Jason R.; Singh, Indresh; Billings, Emily A.; Rush, Margaret; Air, Gillian; Bour, Stephan

doi:10.1016/j.virusres.2021.198545

Cited by 2 publications

(2 citation statements)

References 39 publications

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“…This extension was absent from the Botswana viruses, the Free State ostrich case from 2021, and the 2023 KZN outbreak viruses. This PA-X isoform, designated as PA-X8, was previously also identified in the sequences of least 45 H9N2 subtype viruses in Bangladeshi poultry from 2016–2019, deposited in GenBank [ 33 ]. The phenotypic effect of the PA-X8 isoform of the SA15 viruses remains to be experimentally assessed.…”

Section: Discussionmentioning

confidence: 98%

Outbreaks of H5N1 High Pathogenicity Avian Influenza in South Africa in 2023 Were Caused by Two Distinct Sub-Genotypes of Clade 2.3.4.4b Viruses

Abolnik,

Roberts,

Strydom

et al. 2024

Viruses

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In 2023, South Africa continued to experience sporadic cases of clade 2.3.4.4b H5N1 high-pathogenicity avian influenza (HPAI) in coastal seabirds and poultry. Active environmental surveillance determined that H5Nx, H7Nx, H9Nx, H11Nx, H6N2, and H12N2, amongst other unidentified subtypes, circulated in wild birds and ostriches in 2023, but that H5Nx was predominant. Genome sequencing and phylogenetic analysis of confirmed H5N1 HPAI cases determined that only two of the fifteen sub-genotypes that circulated in South Africa in 2021–2022 still persisted in 2023. Sub-genotype SA13 remained restricted to coastal seabirds, with accelerated mutations observed in the neuraminidase protein. SA15 caused the chicken outbreaks, but outbreaks in the Paardeberg and George areas, in the Western Cape province, and the Camperdown region of the KwaZulu-Natal province were unrelated to each other, implicating wild birds as the source. All SA15 viruses contained a truncation in the PB1-F2 gene, but in the Western Cape SA15 chicken viruses, PA-X was putatively expressed as a novel isoform with eight additional amino acids. South African clade 2.3.4.4b H5N1 viruses had comparatively fewer markers of virulence and pathogenicity compared to European strains, a possible reason why no spillover to mammals has occurred here yet.

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Section: Discussionmentioning

confidence: 98%

Outbreaks of H5N1 High Pathogenicity Avian Influenza in South Africa in 2023 Were Caused by Two Distinct Sub-Genotypes of Clade 2.3.4.4b Viruses

Abolnik,

Roberts,

Strydom

et al. 2024

Viruses

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“…More importantly, the 3 non-structural proteins of EIV include the non-structural protein 1 (NS1), PB1-F2 and PA-X [11,40,41] (Figure 1). These proteins are non-essential for viral replication; however, they play an important role in viral pathogenicity, inflammation, and tissue damage during infection [11,[40][41][42][43][44][45][46]. They are best known for counteracting type I interferons (IFNs), important cytokines in the host defense against viruses through the induction of antiviral effector molecules encoded by IFN-stimulated genes (ISGs) [47].…”

Section: Viral Determinants Of Airway Epithelial Cell Deathmentioning

confidence: 99%

Could Interleukin-33 (IL-33) Govern the Outcome of an Equine Influenza Virus Infection? Learning from Other Species

Rozario

Martínez-Sobrido

McSorley

et al. 2021

Viruses

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Influenza A viruses (IAVs) are important respiratory pathogens of horses and humans. Infected individuals develop typical respiratory disorders associated with the death of airway epithelial cells (AECs) in infected areas. Virulence and risk of secondary bacterial infections vary among IAV strains. The IAV non-structural proteins, NS1, PB1-F2, and PA-X are important virulence factors controlling AEC death and host immune responses to viral and bacterial infection. Polymorphism in these proteins impacts their function. Evidence from human and mouse studies indicates that upon IAV infection, the manner of AEC death impacts disease severity. Indeed, while apoptosis is considered anti-inflammatory, necrosis is thought to cause pulmonary damage with the release of damage-associated molecular patterns (DAMPs), such as interleukin-33 (IL-33). IL-33 is a potent inflammatory mediator released by necrotic cells, playing a crucial role in anti-viral and anti-bacterial immunity. Here, we discuss studies in human and murine models which investigate how viral determinants and host immune responses control AEC death and subsequent lung IL-33 release, impacting IAV disease severity. Confirming such data in horses and improving our understanding of early immunologic responses initiated by AEC death during IAV infection will better inform the development of novel therapeutic or vaccine strategies designed to protect life-long lung health in horses and humans, following a One Health approach.

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Novel isoforms of influenza virus PA-X and PB1-F2 indicated by automatic annotation

Cited by 2 publications

References 39 publications

Outbreaks of H5N1 High Pathogenicity Avian Influenza in South Africa in 2023 Were Caused by Two Distinct Sub-Genotypes of Clade 2.3.4.4b Viruses

Outbreaks of H5N1 High Pathogenicity Avian Influenza in South Africa in 2023 Were Caused by Two Distinct Sub-Genotypes of Clade 2.3.4.4b Viruses

Could Interleukin-33 (IL-33) Govern the Outcome of an Equine Influenza Virus Infection? Learning from Other Species

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