Virulent PB1-F2 residues: effects on fitness of H1N1 influenza A virus in mice and changes during evolution of human influenza A viruses

Alymova, Irina V.; McCullers, Jonathan A.; Kamal, Ram P.; Vogel, Peter; Green, Amanda M.; Gansebom, Shane; York, Ian A.

doi:10.1038/s41598-018-25707-y

Cited by 10 publications

(10 citation statements)

References 53 publications

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“…However, PB1-F2 has dissimilar functions in different virus types/subtypes and hosts, which are determined by its length. Usually, avian influenza viruses have full-length PB1-F2 protein, enabling all functions [44], while classical swine H1N1 and A(H1N1)pdm09 viruses frequently contain truncated PB1-F2 with associated loss of function as seen in TJ/1606/18.…”

Section: Discussionmentioning

confidence: 99%

Human infection with a novel reassortant Eurasian-avian lineage swine H1N1 virus in northern China

Guo

Liu

et al. 2019

Emerging Microbes & Infections

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Influenza A virus infections occur in different species, causing mild to severe respiratory symptoms that lead to a heavy disease burden. Eurasian avian-like swine influenza A(H1N1) viruses (EAS-H1N1) are predominant in pigs and occasionally infect humans. An influenza A(H1N1) virus was isolated from a boy who was suffering from fever and headache and designated as A/Tianjin-baodi/1606/2018(H1N1). Full-genome sequencing and phylogenetic analysis revealed that A/Tianjin-baodi/1606/2018(H1N1) is a novel reassortant EAS-H1N1 containing gene segments from EAS-H1N1 (HA and NA), classical swine H1N1(NS) and A(H1N1)pdm09(PB2, PB2, PA, NP and M) viruses. The isolation and analysis of A/Tianjin-baodi/1606/2018(H1) provide further evidence that EAS-H1N1 poses a threat to human health and greater attention should be paid to surveillance of influenza virus infection in pigs and humans.

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Section: Discussionmentioning

confidence: 99%

Human infection with a novel reassortant Eurasian-avian lineage swine H1N1 virus in northern China

Guo

Liu

et al. 2019

Emerging Microbes & Infections

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“…One reason for the differences in levels of IL-1β production is the ability for activation of the inflammasome complex upon recognition of viral antigen, such as PB1-F2 ( McAuley et al, 2013 ). Interestingly, the inflammasome activation-associated mutation site 79R was observed in the PB1-F2 of all five H9N2 viruses except Hu/04 virus ( Alymova et al, 2018 ) ( Table 1 ). Our results indicated that even LPAI H9N2 viruses replicated well in mice and chickens, and could cause significant increases in pro-inflammatory cytokine expression ( Figure 4A , 5D ).…”

Section: Discussionmentioning

confidence: 99%

H9N2 Viruses Isolated From Mammals Replicated in Mice at Higher Levels Than Avian-Origin Viruses

et al. 2019

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H9N2 subtype influenza A virus (IAV) has more than 20 genotypes that are able to cross species barriers and expand from birds to mammals and humans. To better understand the impact of different H9N2 genotypes and their characteristics, five H9N2 viruses from different hosts including chickens, geese, pigs, mink, and humans representing the B69 88(Gs/14, Ck/15, and Mi/14), B35 (Sw/08) and G9 genotypes (Hu/04) were infected in chicken and mice. In mice, mammal-origin viruses replicated at higher levels in the lungs compared to avian viruses. The goose-virus replicated at the lowest levels indicating poor adaptation. Increased pro-inflammatory cytokines were positively correlated with viral loads in the lung. In chickens, all viruses were excreted from cloacal and/or oropharyngeal swabs. Interestingly, Mink-origin virus exhibited higher virulence and replication in mice and chickens. Our data indicate that mammal-origin H9N2 viruses are more adapted and virulent in mice than the avian-origin viruses.

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“…42,43 Both subtypes and clades probably have intrinsic differences in virulence; for example, due to different receptor preferences or differences in virulenceassociated pro teins. [58][59][60] However, such variations are difficult to distinguish from the effects of immunity acquired through prior infection or vaccination.…”

Section: Diversity Of Influenza Virusesmentioning

confidence: 99%

Immune-mediated attenuation of influenza illness after infection: opportunities and challenges

et al. 2021

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Sterilising immunity that blocks infection for life, and thus prevents illness after infection, is the ultimate goal for vaccines. Neither influenza infection nor vaccination provide sterilising immunity. Mutations during influenza viral genome replication result in the emergence of viruses that evade immunity and cause reinfections. Waning of immunity also results in reinfections to homologous influenza viruses. However, immunity might limit the severity of disease after infection or vaccination (ie, immunoattenuation). We provide a comprehensive examination of experimental and observational peer reviewed evidence since 1933, when the first influenza virus was isolated, on whether immunity blocks subsequent infection or attenuates illness. Although an abundance of experimental evidence supports immunoattenuation, clinical evidence is rudimentary and conflicting. To the extent that immunoattenuation occurs, understanding the varied pathways to illness, pathogenesis, clinical manifestations, and correlates of attenuation can improve the design and evaluation of influenza vaccines. By elucidating the mechanisms of immunoattenuation and phenotypes of illness, we clarify ambiguities and identify unmet needs that, if addressed with priority, could strategically improve the design of vaccines for the prevention of influenza."The chief danger in human influenza lies not in the effect of the virus on the nasal mucosa but in the tendency to lung involvement and if the presence of circulating antibodies is a check upon such pulmonary involvement it is possible that their production in man by vaccine inoculations would have some influence upon the mortality-rate of an epidemic even if it had no influence upon the morbidity." 1

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Virulent PB1-F2 residues: effects on fitness of H1N1 influenza A virus in mice and changes during evolution of human influenza A viruses

Cited by 10 publications

References 53 publications

Human infection with a novel reassortant Eurasian-avian lineage swine H1N1 virus in northern China

Human infection with a novel reassortant Eurasian-avian lineage swine H1N1 virus in northern China

H9N2 Viruses Isolated From Mammals Replicated in Mice at Higher Levels Than Avian-Origin Viruses

Immune-mediated attenuation of influenza illness after infection: opportunities and challenges

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