Publisher Correction: Host and viral determinants of influenza A virus species specificity

Long, Jason S.; Mistry, Bhakti; Haslam, Stuart M.; Barclay, William

doi:10.1038/s41579-018-0140-y

Cited by 11 publications

(10 citation statements)

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“…IVPI tests confirmed that the XL virus had low pathogenicity in chickens. Q/G225D, Q226L, S227N, and G228S mutations in HA proteins have been reported to increase SA-α2,6-Gal binding affinity ( 39 , 40 ). Previous studies showed that H7N9 AIVs with low pathogenicity with residues 186V and 226L on the HA protein bound to SA-α2,6-Gal receptors with high affinity ( 54 ).…”

Section: Discussionmentioning

confidence: 99%

Characterization of an H7N9 Influenza Virus Isolated from Camels in Inner Mongolia, China

et al. 2023

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Section: Discussionmentioning

confidence: 99%

Characterization of an H7N9 Influenza Virus Isolated from Camels in Inner Mongolia, China

et al. 2023

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“…For the efficient infection of human populations from avian reservoirs, AIVs must overcome the species barriers through adaptive evolution [ 33 ]. Multiple adaptive mutations in viral hemagglutinin (HA) and polymerase subunits are recognized to be necessary for the efficient infection of AIVs in their new host, even in humans [ 34 – 37 ].…”

Section: Discussionmentioning

confidence: 99%

Enhanced stability of M1 protein mediated by a phospho-resistant mutation promotes the replication of prevailing avian influenza virus in mammals

Wang

Zong

et al. 2022

PLoS Pathog

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Avian influenza virus (AIV) can evolve multiple strategies to combat host antiviral defenses and establish efficient infectivity in mammals, including humans. H9N2 AIV and its reassortants (such as H5N6 and H7N9 viruses) pose an increasing threat to human health; however, the mechanisms involved in their increased virulence remain poorly understood. We previously reported that the M1 mutation T37A has become predominant among chicken H9N2 isolates in China. Here, we report that, since 2010, this mutation has also been found in the majority of human isolates of H9N2 AIV and its emerging reassortants. The T37A mutation of M1 protein enhances the replication of H9N2 AIVs in mice and in human cells. Interestingly, having A37 instead of T37 increases the M1 protein stability and resistance to proteasomal degradation. Moreover, T37 of the H9N2 M1 protein is phosphorylated by protein kinase G (PKG), and this phosphorylation induces the rapid degradation of M1 and reduces viral replication. Similar effects are also observed in the novel H5N6 virus. Additionally, ubiquitination at K187 contributes to M1-37T degradation and decreased replication of the virus harboring T37 in the M1 protein. The prevailing AIVs thereby evolve a phospho-resistant mutation in the M1 protein to avoid viral protein degradation by host factors, which is advantageous in terms of replication in mammalian hosts.

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“…The HA is a major factor for host specificity (35, 36) and is a prime target for evolution as a human seasonal virus adapts to the swine host. Specific amino acid substitutions at or near the RBS have been shown to alter receptor binding or antigenicity of influenza viruses (5, 37, 38), which likely affects host specificity.…”

Section: Discussionmentioning

confidence: 99%

Transmission of human influenza A virus in pigs selects for adaptive mutations on the HA gene

Abente

Sutton

et al. 2022

Preprint

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Influenza A viruses (IAV) cause respiratory diseases in many host species, including humans and pigs. The spillover of IAV between swine and humans has been a concern for both public health and the swine industry. With the emergence of the triple reassortant internal gene (TRIG) constellation, establishment of human-origin IAVs in pigs has become more common, leading to increased viral diversity. However, little is known about the adaptation processes that are needed for a human-origin IAV to transmit and become established in pigs. We generated a reassortant IAV containing surface gene segments from a human IAV strain and internal gene segments from the 2009 pandemic and TRIG IAV lineages and demonstrated that it can replicate and transmit in pigs. Sequencing and variant calling analysis identified a mutant that emerged during replication in pigs, which was mapped to a region near the receptor binding site of the hemagglutinin (HA). The variant was present in all contact pigs and replicated more efficiently in differentiated swine tracheal cells compared to the virus containing the wildtype human-origin HA. These results show that variants are selected quickly after replication of human-origin HA in pigs, leading to improved fitness in the swine host, likely contributing to transmission.ImportanceInfluenza A viruses (IAV) cause respiratory disease in several species, including humans and pigs. The bidirectional transmission of IAV between humans and pigs plays a significant role in the generation of novel viral strains, greatly impacting viral epidemiology. However, little is known about the evolutionary processes that allow human IAV to become established in pigs. In this study, we generated reassortant viruses containing human seasonal HA and NA on different constellations of internal genes and tested their ability to replicate and transmit in pigs. We demonstrated that a virus containing a common internal gene constellation currently found in U.S. swine was able to transmit efficiently via the respiratory route. We identified a specific amino acid mutation that was fixed in the respiratory contact pigs that was associated with improved replication in primary swine tracheal epithelial cells, suggesting it was crucial for the transmissibility of the human virus in pigs.

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Publisher Correction: Host and viral determinants of influenza A virus species specificity

Cited by 11 publications

References 0 publications

Characterization of an H7N9 Influenza Virus Isolated from Camels in Inner Mongolia, China

Characterization of an H7N9 Influenza Virus Isolated from Camels in Inner Mongolia, China

Enhanced stability of M1 protein mediated by a phospho-resistant mutation promotes the replication of prevailing avian influenza virus in mammals

Transmission of human influenza A virus in pigs selects for adaptive mutations on the HA gene

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