Conclusion: A similar phenomenon was observed in patients infected with the HA D222G mutant of influenza A(H1N1)pdm09 virus; this virus showed preferential replication in the lower respiratory tract and this infection was correlated with severe outcomes or deaths.
HA222 polymorphism in Influenza A(H1N1) 2009 isolates from Intensive Care Units and ambulatory patients during three influenza seasons.
Abstract: Amino acid substitutions which can affect the receptor binding specificity of the influenza virus, like the substitution of aspartic acid with glycine in position 222 of the haemagglutinin (HA) of influenza virus A(H1N1) 2009, have been associated with increased viral pathogenicity and increased tropism for the lower respiratory tract.
Evaluation of HA-D222G/N polymorphism using targeted NGS analysis in A(H1N1)pdm09 influenza virus in Russia in 2018-2019.
Abstract: Altogether, our data suggest that the HA D222G substitution in the K/09 virus might be deleterious to viral fitness.
Abstract: Compared with the A/Korea/01/2009 (K/09) virus, the HA D222G mutant showed reduced growth in cells and reduced binding avidity to human and turkey red blood cells.
Abstract: In a BALB/c mouse infection model, infection with the HA D222G mutant virus resulted in less body weight loss when compared to the parental K/09 virus.
Abstract: In this study, we have investigated the pathogenic effects of the HA D222G substitution in a 2009 pandemic H1N1 virus in mice.
Abstract: Recently, there have been multiple cases of severe human infectio
Functional balance between the hemagglutinin and neuraminidase of influenza A(H1N1)pdm09 HA D222 variants.
Abstract: D222G/N substitutions in A(H1N1)pdm09 hemagglutinin may be associated with increased binding of viruses causing low respiratory tract infections and human pathogenesis.
Introduction: In mouse models, conflicting results have been reported, with some suggesting that D222G H1N1pdm viruses acquire an enhanced pathogenicity while others fail to display evidence of such an effect.
Introduction: Preliminary epidemiological studies from Norway reported a higher frequency of the D222G mutation in hemagglutinin (HA, H1 numbering) of influenza viruses cultured from severe cases compared with mild cases.
Introduction: Previous studies have indicated that the D222G substitution influenced the receptor binding specificity of th
Accumulation of human-adapting mutations during circulation of A(H1N1)pdm09 influenza virus in humans in the United Kingdom.
Discussion: In our MOSAIC hospitalized cohort, we did not detect the specific HA mutations described by others to affect A(H1N1)pdm09 virulence, for example, HA D222G, which purportedly facilitates better binding to alpha-2,3-sialic acid-linked receptors in the lower respiratory tract, changes in glycosylation, or antigenicity were not present.
Discussion: Other groups have suggested that HA D222G is relatively common in severe cases.The D222G mutation has been suggested to sometimes arise during virus culture as an artifact and may also only be present as a minority variant in samples taken at certain times during the infection.
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
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 D222N, which was observed in isolates 19/2010 and 20/2010, is more frequent among fatal cases of the disease in humans.37 However, the animals from which those viruses were isolated did not show signs of severe disease.
Clinical and molecular characteristics of the 2009 pandemic influenza H1N1 infection with severe or fatal disease from 2009 to 2011 in Shenzhen, China.
Abstract: In most of the D222G cases (11/13), the mutant virus was found as a quasispecies.
Abstract: No D222G mutations were found among the 381 mild cases.
Abstract: The association between a particular mutation in the HA1 subunit of the influenza virus haemagglutinin, D222G, and severe and fatal disease in cases of influenza A(H1N1)pdm09 in Norway during the 2009 pandemic was investigated using pyrosequencing.
Influenza virus A(H1N1)pdm09 hemagglutinin polymorphism and associated disease in southern Germany during the 2010/11 influenza season.
Abstract: The D222G mutation, which had previously been observed in severe cases, was not detected.
Introduction: The D222G mutation in the receptor-binding domain of the HA gene has been linked to severe cases.
Discussion: Clinically, the mutations D222G and N have been associated with a more virulent phenotype.
Discussion: No D222G change was observed here.
Identification of critical residues in the hemagglutinin and neuraminidase of influenza virus H1N1pdm for vaccine virus replication in embryonated chicken eggs.
Abstract: In 2009, we successfully produced a high-yield live attenuated H1N1pdm A/California/7/2009 vaccine (CA/09 LAIV) by substitution of three residues (K119E, A186D, and D222G) in the hemagglutinin (HA) protein.
IV mutation literature information.
PMID: 
2014
Emerging infectious diseases
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