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.
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.
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.
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.
Conclusion: Furthermore, compound 18 showed strong activity against the A/PR/8/34 strain, an A/H1N1 virus with two mutations (S31N and V27T) in the M2 protein.
Table: S31N
Figure: The IC50 values denote the reported 50% inhibitory concentrations on A/M2 wt,
Characterization of the amantadine-resistant H5N1 highly pathogenic avian influenza variants isolated from quails in Southern China.
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.
IV mutation literature information.
PMID: 
2015
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