literature

IV mutation literature information.

Clinical and molecular characteristics of the 2009 pandemic influenza H1N1 infection with severe or fatal disease from 2009 to 2011 in Shenzhen, China.

PMID: 23280524 2013 Journal of medical virology

Abstract: Both D222G and D222N were associated statistically with severe disease.

Abstract: Four substitutions (D222G, D222N, D222E, and Q223R) were observed on the 220-loop of the receptor-binding sites of the HA gene.

Genetic characterization of influenza virus circulating in Brazilian pigs during 2009 and 2010 reveals a high prevalence of the pandemic H1N1 subtype.

PMID: 23280098 2013 Influenza and other respiratory viruses

Result: All 2009-2010 Brazilian swine and human isolates contained residues of the swine lineage in the receptor-binding pockets, with no substitutions in those sites relative to the A/Mexico/4108/09 strain, except for the substitutions A134T and D222N in isolates A/swine/Brazil/19/2010 and A/swine/Brazil/20/2010.

Discussion: It has been demonstrated that pandemic H1N1 2009 evolved and shifted from an initial mixed clade pattern to a clade 7-predominant pattern.34 The subsequent selection and evolution of clade 7 resulted in the circulation of variants D222G/N or E.35 Mutation D222G in the hemagglutinin protein has been correlated with the clinical onset of disease, and it was frequently found in severe/fatal cases of the pandemic influenza in humans.36 Likewise, the substitution D222

Detection of haemagglutinin D222 polymorphisms in influenza A(H1N1)pdm09-infected patients by ultra-deep pyrosequencing.

PMID: 22862843 2013 Clinical microbiology and infection

Abstract: D222E, D222G, D222N and D222A were observed in 37.0%, 11.1%, 7.4% and 3.7% of patients, respectively; 10.7% of samples harboured more than two variants.

Abstract: D222G/N/A were detected, as either minor or predominant variants, only in severe cases, whereas D222E was equally represented in severe and moderate-mild infections.

Frequency of D222G and Q223R hemagglutinin mutants of pandemic (H1N1) 2009 influenza virus in Japan between 2009 and 2010.

PMID: 22363521 2012 PloS one

Discussion: In this study, D222E, D222N, and D222V variants were not detected, even when deep sequencing was performed (Table S1).

Nationwide molecular surveillance of pandemic H1N1 influenza A virus genomes: Canada, 2009.

PMID: 21249207 2011 PloS one

Discussion: For example, HA D222E/G/N (also called 239) and HA Q293H (also called 310) mutant viruses have been isolated worldwide from fatal laboratory-confirmed A/H1N1pdm cases.

[Detection of amino acid substitutions of asparaginic acid for glycine and asparagine at the receptor-binding site of hemagglutinin in the variants of pandemic influenza A/H1N1 virus from patients with fatal outcome and moderate form of the disease].

PMID: 20608076 2010 Voprosy virusologii

Abstract: This site exhibited mutations in 9 samples: D222G (n=3), D222N (n=3), and D222G/D222N (n=3).

[A possible association of fatal pneumonia with mutations of pandemic influenza A/H1N1 sw1 virus in the receptor-binding site of the HA1 subunit].

PMID: 20886705 2010 Voprosy virusologii

Abstract: 70% of the primary materials from the deceased patients were found to have pandemic influenza A(H1N1) v mutants in the lung tissue with D222G (15%), D222N (15%), D222E (2%) substitutions, as well as a mixture of mutants (38%).

Abstract: Preliminary data from the study of the interaction of the hemagglutinin of two strains having D222G and D222N mutations with 9 oligosaccharides imitating the variants of cell receptors for influenza A virus suggest that there is a double receptor specificity for alpha2'-3' and alpha2'-6'-sialosides with a preponderance of alpha2'-3'-specificity.

Epidemiological, demographic, and molecular characteristics of laboratory-confirmed pandemic influenza A (H1N1) virus infection in Turkey, May 15-November 30, 2009.

PMID: 20657062 2010 Japanese journal of infectious diseases

Abstract: More than 37% of the isolates had mutation at position D222E/N on HA gene.

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