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 IV mutation literature information.


  [Genetic Diversity and Evolution of the M Gene of Human Influenza A Viruses from 2009 to 2013 in Hangzhou, China].
 PMID: 26164939       2015       Bing du xue bao
Abstract: All strains contained the adamantine-resistant mutation S31N in its M2 protein.
Abstract: One of the seasonal A(H3N2) viruses had another form of double-mutant R45H/S31N.
Abstract: Two of the A(H1N1)pdm09 strains had double mutants of V27A/S31N or V271/S31N.


  Isocyanides as Influenza A Virus Subtype H5N1 Wild-Type M2 Channel Inhibitors.
 PMID: 26506405       2015       ChemMedChem
Abstract: Furthermore, the isocyanide analogues synthesized in this study did not inhibit the V27A or S31N mutant M2 ion channels, according to electrophysiology experiments, and did not exhibit activity against amantadine-resistant virus strains.


  Influenza A(H6N1) Virus in Dogs, Taiwan.
 PMID: 26583707       2015       Emerging infectious diseases
Method: In the M2 protein, A/canine/Taiwan/E01/2014 had an S31N substitution, which suggested resistance to admantanes .
Table: S31N


  Emergence of a novel drug resistant H7N9 influenza virus: evidence based clinical potential of a natural IFN-alpha for infection control and treatment.
 PMID: 24350808       2014       Expert review of anti-infective therapy
Abstract: The emerging H7N9 viruses are resistant to the M2-ion channel blockers because of a S31N mutation in the M2 protein; additionally, some H7N9 isolates have gained neuraminidase R292K substitution resulting in broad resistance to neuraminidase inhibitors.


  Unique reassortant of influenza A(H7N9) virus associated with severe disease emerging in Hong Kong.
 PMID: 24576826       2014       The Journal of infection
Result: The M2 protein contains the S31N mutation which confers resistance to adamantanes.


  Isolation and characterization of H9N2 influenza virus isolates from poultry respiratory disease outbreak.
 PMID: 24790833       2014       SpringerPlus
Abstract: Isolate 1 has the S31N substitution in the M2 gene that has been associated with drug resistance as well as R57Q and C241Y mutations in the NP gene which are associated with human adaptation.
Discussion: Isolate 1 from this study has the S31N substitution, which has also been identified in H9N2 viruses from Iran, UAE and Qatar (Fusaro et al.).
Discussion: The M2 gene has been extensively studied for drug resistance several mutations are known to confer drug resistance; L26F, V27A, A30T, S31N, G34E, L38F (Schnell and Chou).


  Research/review: Structure and linkage disequilibrium analysis of adamantane resistant mutations in influenza virus m2 proton channel.
 PMID: 24909420       2014       Current drug metabolism
Abstract: After evolutionary and linkage disequilibrium analyses, we found that the some residues in the C-terminal were associated with the famed resistant mutation S31N.


  Analysis of the full-length genome of a novel strain of the H7N9 avian influenza virus.
 PMID: 24940441       2014       Experimental and therapeutic medicine
Result: The S31N mutation of the M2 protein encoded by the MP gene was identified in the 52 new H7N9 virus strains.


  Easily accessible polycyclic amines that inhibit the wild-type and amantadine-resistant mutants of the M2 channel of influenza A virus.
 PMID: 24941437       2014       Journal of medicinal chemistry
Abstract: Inhibition of the wild-type M2 channel and the A/M2-S31N, A/M2-V27A, and A/M2-L26F mutant forms of the channel were measured in Xenopus oocytes using two-electrode voltage clamp assays.
Abstract: None of the compounds was found to inhibit the S31N mutant ion channel.
Introduction: During the past years, our group has synthesized several polycyclic Amt analogues containing different scaffolds, including ring-contracted, ring-rearranged, and 2,2-dialkyl derivatives of Amt.- Several of them displayed similar IC50 values for wt A/M2 as Amt but, unfortunately, were inactive against the Amt-resistant S31N or  PMID: 24993865       2014       Virus genes
Abstract: Molecular analysis suggested that QA viruses and clade 4 H5N1 viruses carried consistent residue signatures, such as the characteristic M2 Ser31Asn amantadine-resistance mutation, implying a common origin of these viruses.
Abstract: Results from amantadine sensitivity tests of wild-type QA viruses and their reverse genetic viruses demonstrated that all QA viruses were resistant to amantadine, and the M2 Ser31Asn mutation was determined as the most likely cause of the increased amantadine-resistance of H5N1 QA viruses.



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