Diversity of influenza viruses in swine and the emergence of a novel human pandemic influenza A (H1N1)

Division of Virology, Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Influenza and Other Respiratory Viruses (Impact Factor: 1.9). 09/2009; 3(5):207-13. DOI: 10.1111/j.1750-2659.2009.00096.x
Source: PubMed

ABSTRACT The novel H1N1 influenza virus that emerged in humans in Mexico in early 2009 and transmitted efficiently in the human population with global spread has been declared a pandemic strain. Here we review influenza infections in swine since 1918 and the introduction of different avian and human influenza virus genes into swine influenza viruses of North America and Eurasia. These introductions often result in viruses of increased fitness for pigs that occasionally transmit to humans. The novel virus affecting humans is derived from a North American swine influenza virus that has acquired two gene segments [Neuraminidase (NA) and Matrix (M)] from the European swine lineages. This reassortant appears to have increased fitness in humans. The potential for increased virulence in humans and of further reassortment between the novel H1N1 influenza virus and oseltamivir resistant seasonal H1N1 or with highly pathogenic H5N1 influenza stresses the need for urgent pandemic planning.

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    • "Genetic analysis confirmed that it was a triple reassorted virus from human, swine, and avian lineages. The virus carried the HA, NP, and NS genes of classical swine virus origin, the PB2 and PA genes from North American avian viruses, the PB1 gene from viruses of human origin and the NA and M genes from Eurasian swine avian-like viruses [Brockwell-Staats et al., 2009; Garten et al., 2009; Peiris et al., 2009]. Molecular analysis of A(H1N1)pdm09 strains had classified them into seven discrete genetic clades [Nelson et al., 2009] which were also confirmed by several "
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    ABSTRACT: The pandemic H1N1 strain of Influenza A virus [A(H1N1)pdm09] is now well adapted in human populations. However, it is still causing sporadic outbreaks worldwide with different severity. The present study was planned to understand the genetic diversity (based on the HA1 gene) of influenza A(H1N1)pdm09 strains circulating during the post pandemic period. The HA1 gene was selected because the HA1 protein is immunogenic, functions as a receptor binding site and indirectly affects transmission and pathogenicity of virus. A total of 2,818 cases were enrolled. Nasal/throat swabs from all cases were tested by one-step real time PCR for detection of influenza virus types and subtypes according to the CDC protocol. Of these, 134 cases were A(H1N1)pdm09 positive, 34 of which were screened for HA1 gene (position 434–905) sequencing (Big-Dye terminator using 3130 ABI, Genetic analyzer). Molecular and phylogenetic analysis was performed using PhyML approach (v. 3.0). All A(H1N1)pdm09 positive and negative cases were clinically characterized. Phylogentically, all Lucknow strains (n = 33) except one fall with the clade seven reference strain. One strain showed 99.9% similarities with clade one reference strain A/California/07/2009. In mutational analysis, 33 strains had the S220T mutation, which is at an antigenic site and characteristic of clade seven along with few minor mutations; K180I/T/Q, V190I, S200P, S202T, A203T, A214T, S220T, V251I, and A273T. These results suggest that clade seven was the most widely circulating clade in Lucknow and A(H1N1)pdm09 cases showed mild clinical symptoms as compared to A(H3N2) or influenza B cases. J. Med. Virol. © 2014 Wiley Periodicals, Inc.
    Journal of Medical Virology 04/2014; DOI:10.1002/jmv.23946 · 2.22 Impact Factor
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    • "It appears clear that the pandemic (H1N1) 2009 virus arose from a reassortment between North American and Eurasian swine viruses (Garten et al., 2009; Smith et al., 2009a,b); both the North American and the Eurasian immediate progenitors of the pandemic virus itself originated from at least two reassortments. One salient feature of this paper is its comprehensive information regarding the subtypes, contributing gene segments, and the time of emergence of the previous reassortants, which are provided through a careful review of published analyses and additional analyses of sequences collected during the entire pandemic period, available in GenBank (Fig. 1) (Brockwell-Staats et al., 2009; Garten et al., 2009; Gibbs et al., 2009; Smith et al., 2009a,b; Trifonov et al., 2009). In addition, our analyses further confirmed that the precursors of the pandemic H1N1 virus went unnoticed or unsampled in swine herds for 9–12 years for the six North American swine influenza viral genes and 12–17 years for the two Eurasian genes (NA and MP) (Gibbs et al., 2009; Smith et al., 2009a,b; Trifonov et al., 2009); this strongly suggests that increased surveillance is critical in swine herds in order to prevent a future event like the 2009 H1N1 pandemic. "
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    ABSTRACT: The pandemic (H1N1) 2009 virus is unique in many aspects, especially in its genetics and evolution. In this paper, we examine the molecular mechanisms underlying the evolution of this novel virus through a comprehensive bioinformatics analysis, and present results in the context of a review of the literature. The pandemic virus was found to arise from a reassortment of two swine viruses, each of which ultimately arose from interspecies transmission. It experienced fast evolutionary rates and strong selection pressures, diverging into two different clusters at the early pandemic stage. Cluster I became extinct at the end of 2009 whereas Cluster II continued to circulate at much lower rates in 2010. Therefore, on August 10 of 2010 the WHO declared the end of the pandemic. Important mutations associated with host specificity, virulence, and drug resistance were detected in the pandemic virus, indicating effective transmission and increased severity in humans. Much has been learned about the evolutionary dynamics of this pandemic virus; however, it is still impossible to predict when the next pandemic will occur and which virus will be responsible. Improved surveillance at different levels (both national and international) and in different hosts (especially in swine) appears to be crucial for early detection and prevention of future influenza pandemics.
    Infection, genetics and evolution: journal of molecular epidemiology and evolutionary genetics in infectious diseases 03/2011; 11(5):803-11. DOI:10.1016/j.meegid.2011.02.021 · 3.26 Impact Factor
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    • "Influenza was first described as a disease of swine in 1918 (Koen, 1919). The first influenza A virus was isolated from swine in 1930 (Brockwell-Staats et al., 2009). A swine influenza virus was isolated from a human in 1974, from 1974 to 2005; there were 43 confirmed cases of transmission of influenza A virus from pigs to humans reported, with six fatalities (Brockwell- Staats et al., 2009). "
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    ABSTRACT: The swine flu is an infectious disease of swine and human,causing a huge amount of death to both. The aim ofthis study was to analyse the mutation possibility of swineinfluenza virus sub-type A/Swine/Nebraska/(H1N1) fromswine of Nebraska. The H1N1 amino acid sequences ofneuraminidase (GenBank Acc. No: ABR28650) and hemagglutinin(GenBank Acc. No: ABR28647) were analyzedfor mutations using BLASTP and ClustalW programs.Our in silico analysis predicted that hemagglutininand neuraminidase of swine influenza virus are sensitiveto mutations at positions 225, 283 and 240, 451 respectively.These mutations were significant for its pathogenicnature because they are involved in change in polarity orhydrophobicity. Domain and motif search shows that mutationswere detected in NA (T240A, G451S) and HA(I283V) at a predicted site of N-myristoylation. Secondarystructure analysis predicted that no structural conformationchanges were observed in HA and NA at positions225, 283 and 240, 451 respectively. The programPROTMUTATION was developed in Perl CGI programmingusing Needleman-Wunsch algorithm for global sequencealignment. This program was used to monitor themutations and predicts the trend of mutations.
    Journal of Proteomics & Bioinformatics 01/2010; 03(02):055-060. DOI:10.4172/jpb.1000121
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