Amino acid substitution D222N from fatal influenza infection affects receptor-binding properties of the influenza A(H1N1)pdm09 virus

Matos-Patrón, A.; Byrd-Leotis, Lauren; Steinhauer, David A.; Barclay, William; Ayora-Talavera, Guadalupe

doi:10.1016/j.virol.2015.05.012

Cited by 10 publications

(6 citation statements)

References 31 publications

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“…The N188D substitution, located at the receptor-binding region (190 helix) of HA protein ( Figure 3 ), is a notable replacement ( Skehel and Wiley, 2000 ). A recent study revealed that alterations of amino acid at this site have significant effects on the binding capacity of A(H1N1)pdm09 ( Matos-Patron et al, 2015 ). In addition, N188D, G146S, and V242I mutations are located at the antigenic epitope B, antigenic epitope A, and antigenic epitope D of the HA protein, respectively ( Figure 3 ), where substitutions at these sites may lead to antigenic drift in IAVs and the subsequent evasion of host immune responses ( Shih et al, 2007 ).…”

Section: Resultsmentioning

confidence: 99%

Host Adaptive Evolution of Avian-Origin H3N2 Canine Influenza Virus

et al. 2021

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Since its first isolation in around 2007, the avian-origin H3N2 canine influenza virus (CIV) has become established and continues to circulate in dog populations. This virus serves as a useful model for deciphering the complex evolutionary process of interspecies transmission of influenza A virus (IAV) from one species to its subsequent circulation in another mammalian host. The present investigation is a comprehensive effort to identify and characterize genetic changes that accumulated in the avian-origin H3N2 CIV during its circulation in the dog. We revealed that H3N2 CIV experiences greater selection pressure with extremely high global non-synonymous to synonymous substitution ratios per codon (dN/dS ratio) for each gene compared to the avian reservoir viruses. A total of 54 amino acid substitutions were observed to have accumulated and become fixed in the H3N2 CIV population based on our comprehensive codon-based frequency diagram analysis. Of these substitutions, 11 sites also display high prevalence in H3N8 CIV, indicating that convergent evolution has occurred on different lineages of CIV. Notably, six substitutions, including HA-G146S, M1-V15I, NS1-E227K, PA-C241Y, PB2-K251R, and PB2-G590S, have been reported to play imperative roles in facilitating the transmission and spillover of IAVs across species barriers. Most of these substitutions were found to have become fixed in around 2015, which might have been a favorable factor that facilitating the spread of these CIV lineages from South Asia to North America and subsequent further circulation in these areas. We also detected 12 sites in six viral genes with evidence for positive selection by comparing the rates of non-synonymous and synonymous substitutions at each site. Besides, our study reports trends of enhanced ongoing adaptation of H3N2 CIV to their respective host cellular systems, based on the codon adaptation index analysis, which points toward increasing fitness for efficient viral replication. In addition, a reduction in the abundance of the CpG motif, as evident from an analysis of relative dinucleotide abundance, may contribute to the successful evasion of host immune recognition. The present study provides key insights into the adaptive changes that have accumulated in the avian-origin H3N2 viral genomes during its establishment and circulation into dog populations.

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Section: Resultsmentioning

confidence: 99%

Host Adaptive Evolution of Avian-Origin H3N2 Canine Influenza Virus

et al. 2021

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“…Various anatomical sites and cell types may exert differing degrees of selective pressure favoring α-2,3- or α-2,6-tropic viruses ( Lakdawala et al., 2015 ). HA 225N was identified in severe human infections during the 2009 H1N1 pandemic ( Kong et al., 2014 , Mak et al., 2010 , Matos-Patrón et al., 2015 , Wu et al., 2013 ). It enables binding to both α-2,6 and α-2,3 receptors and increases binding to non-sialylated glycans ( Matos-Patrón et al., 2015 ).…”

Section: Resultsmentioning

confidence: 99%

“…HA 225N was identified in severe human infections during the 2009 H1N1 pandemic ( Kong et al., 2014 , Mak et al., 2010 , Matos-Patrón et al., 2015 , Wu et al., 2013 ). It enables binding to both α-2,6 and α-2,3 receptors and increases binding to non-sialylated glycans ( Matos-Patrón et al., 2015 ). Diversity at position 225 may therefore be maintained due to balancing selection, which preserves multiple beneficial alleles in a population.…”

Section: Resultsmentioning

confidence: 99%

Selective Bottlenecks Shape Evolutionary Pathways Taken during Mammalian Adaptation of a 1918-like Avian Influenza Virus

Moncla

Zhong

Nelson

et al. 2016

Cell Host & Microbe

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Summary Avian influenza virus reassortants resembling the 1918 human pandemic virus can become transmissible among mammals by acquiring mutations in hemagglutinin (HA) and polymerase. Using the ferret model, we trace the evolutionary pathway by which an avian-like virus evolves the capacity for mammalian replication and airborne transmission. During initial infection, within-host HA diversity increased drastically. Then, airborne transmission fixed 2 polymerase mutations that do not confer a detectable replication advantage. In later transmissions, selection fixed advantageous HA1 variants. Transmission initially involved a “loose” bottleneck, which became strongly selective after additional HA mutations emerged. The stringency and evolutionary forces governing between-host bottlenecks may therefore change throughout host adaptation. Mutations occurred in multiple combinations in transmitted viruses, suggesting that mammalian transmissibility can evolve through multiple genetic pathways despite phenotypic constraints. Our data provide a glimpse into avian influenza virus adaptation in mammals, with broad implications for surveillance on potentially zoonotic viruses.

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“…However, the potential for a virus to emerge and spread widely in human or swine populations is likely to be a multi-genic trait comprising factors beyond just antigenicity ( Trock et al, 2012 ). These factors include receptor binding ( Matos-Patrón et al, 2015 ; Elderfield et al, 2014 ), adaptations to the matrix, non-structural, and neuraminidase proteins ( Elderfield et al, 2014 ) as well as other factors differing between human and swine influenza viruses yet to be identified. There is also a need to better understand the competition dynamics of different influenza virus variants and subtypes in both human and swine populations and how these dynamics affect the potential for invasion by novel viruses.…”

Section: Discussionmentioning

confidence: 99%

The global antigenic diversity of swine influenza A viruses

Lewis

Russell

Langat

et al. 2016

eLife

168

173

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Swine influenza presents a substantial disease burden for pig populations worldwide and poses a potential pandemic threat to humans. There is considerable diversity in both H1 and H3 influenza viruses circulating in swine due to the frequent introductions of viruses from humans and birds coupled with geographic segregation of global swine populations. Much of this diversity is characterized genetically but the antigenic diversity of these viruses is poorly understood. Critically, the antigenic diversity shapes the risk profile of swine influenza viruses in terms of their epizootic and pandemic potential. Here, using the most comprehensive set of swine influenza virus antigenic data compiled to date, we quantify the antigenic diversity of swine influenza viruses on a multi-continental scale. The substantial antigenic diversity of recently circulating viruses in different parts of the world adds complexity to the risk profiles for the movement of swine and the potential for swine-derived infections in humans.DOI: http://dx.doi.org/10.7554/eLife.12217.001

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Amino acid substitution D222N from fatal influenza infection affects receptor-binding properties of the influenza A(H1N1)pdm09 virus

Cited by 10 publications

References 31 publications

Host Adaptive Evolution of Avian-Origin H3N2 Canine Influenza Virus

Host Adaptive Evolution of Avian-Origin H3N2 Canine Influenza Virus

Selective Bottlenecks Shape Evolutionary Pathways Taken during Mammalian Adaptation of a 1918-like Avian Influenza Virus

The global antigenic diversity of swine influenza A viruses

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