Molecular basis of the receptor binding specificity switch of the hemagglutinins from both the 1918 and 2009 pandemic influenza A viruses by a D225G substitution.
PMID: 20367331
2010
The Journal of infectious diseases
Abstract: D225G quasispecies were identified mainly in endotracheal aspirate samples and were identified less frequently in nasopharyngeal aspirate samples from patients with severe disease.
Abstract: Direct analysis of polymorphisms in 126 amino acids spanning the receptor-binding site in the hemagglutinin of pandemic H1N1 2009 virus from 117 clinical specimens in Hong Kong found the D225G substitution for 7 (12.5%) of 57 patients with severe disease and for 0 (0%) of 60 patients with mild disease.
Abstract: The D225G (aspartic acid to glycine) substitution in the hemagglutinin of H1N1 influenza virus may alter its receptor-binding specificity.
Inhibition of neuraminidase inhibitor-resistant influenza virus by DAS181, a novel sialidase fusion protein.
Result: Non-conserved mutations at these two positions, N163K/H and D225G, thus may be sufficient to cause reduced sensitivity to NAIs in MDCK cells.
Discussion: Similarly in our study, the 2007 and 2009 isolates that are resistant to oseltamivir and have reduced sensitivity to zanamivir carry mutations in both NA (H274Y) and HA (N163K/T/H and D225G), but the observed HA mutations have not been reported previously in drug-resistant IFV strains.
Treatment of influenza A (H1N1) virus infections in mice and ferrets with cyanovirin-N.
Abstract: Recently we created a hybrid (reassortant) influenza A/WSN/33 (H1N1) virus containing the
Method: The Asp225Gly mutation was introduced in the HA gene encoding the HA1 subunit by PCR based site-directed mutagenesis.
Method: The recombinant virus was designated influenza A/WSN/33 HAnc-Asp225Gly (H1N1).
Method: They were infected intranasally (i.n.) with approximately 1 x 103 cell culture infectious doses (CCID50) of influenza A/WSN/33 HAnc-Asp225Gly (H1N1) virus per mouse in a 50-mul inoculum volume.
Result: Mice infected with the influenza A/WSN/33 HAnc-Asp225Gly (H1N1) virus were treated with doses of CV-N starting 4 h prior to virus exposure (Table 1).
IV mutation literature information.
PMID: 
2010
The Journal of infectious diseases
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