Conclusion: However, our recent studies demonstrated that unlike amantadine, M2-S31N channel blockers have a higher genetic barrier of drug resistance that is comparable to oseltamivir.
Conclusion: In addressing this unmet medical need, we revisited the M2 proton channel and aim to develop the next generation of antivirals by targeting the M2-S31N mutant.
Conclusion: In this study, we developed a late-stage diversification synthesis strategy that enabled us to expeditiously synthesize a focused library of M2-S31N inhibitors.
Conclusion: It was found that a hydrophobic substitution, preferentially piperidine and azepane, is required at the para-position of the aromatic head group for potent M2-
Sensitive Detection and Simultaneous Discrimination of Influenza A and B Viruses in Nasopharyngeal Swabs in a Single Assay Using Next-Generation Sequencing-Based Diagnostics.
Abstract: Of the influenza A viruses, 66.7% of A(H3N2) viruses tested had a E627K mutation in the PB2 protein, and 87.8% of the influenza A viruses contained the S31N mutation in the M2 protein.
Introduction: Current methods that evaluate antiviral resistance require two independent tests for the S31N substitutions conferring amantadine-resistance and the H274Y substitution conferring oseltamivir-resistance.
Discussion: Sequence analysis of 123 influenza A viruses revealed that 66.7%(82/123) of A(H3N2) viruses had a single signature mutation of E627K in the PB2 protein, and 88%(108/123) of influenza A(H3N2 and pdH1N1) viruses contained the S31N mutation in the
Endemic Variation of H9N2 Avian Influenza Virus in China.
Abstract: A total of 96.8% (337/348) of the viruses had three amino-acid deletions at 63-65 in the NA stalk, associated with enhanced virulence in chickens and mice; 97.1% (338/348) of M2 proteins had the S31N mutation associated with adamantane resistance in humans.
Characterization of drug-resistant influenza A(H7N9) variants isolated from an oseltamivir-treated patient in Taiwan.
PMID: 25124927
2015
The Journal of infectious diseases
Result: The Taiwan/1 viruses contained M2-S31N, a marker of resistance to M2 blockers found in all 2013-2014 influenza A(H7N9) viruses.
Identification of novel compounds against an R294K substitution of influenza A (H7N9) virus using ensemble based drug virtual screening.
PMID: 25589893
2015
International journal of medical sciences
Introduction: The most remarkable mutation is in S31N position that maintains the function of M2 channel in the present of adamantine drugs.
Introduction: Unexpectedly, all novel influenza A H7N9 viruses possess the mutation S31N in M2 protein channel and N9 serotype (designated as A/Shanghai/1/2013) encoded for R294K mutation.
Influenza A viruses of swine circulating in the United States during 2009-2014 are susceptible to neuraminidase inhibitors but show lineage-dependent resistance to adamantanes.
Result: By tracing the history of this particular position, we found that the S31N-M2 represents 83% of all changes that occur at this position across the phylogeny, suggesting that this mutation has a high probability of emerging randomly.
Result: Our analysis suggested that the fixation of the S31N mutation in the IAV-S population occurred as early as 1998.8, but it was not detected in the IAV-S population until 2009.
Result: Regardless, our results show that the emergence and rapid spread of the S31N-M2 amantadine-resistant IAV-S in the U.S.
Result: occurred after the S31N-M2 IAV-S became established in the swine population.
PB2 segment promotes high-pathogenicity of H5N1 avian influenza viruses in mice.
Method: The frequencies of the appearance of recognized adamantine resistance-associated amino acids (L26F, V27A, A30T, A30V, S31N, G34E, and L38F) were identified and tabulated.
Result: Adamantane-resistant mutations (L26F, V27A, A30T, S31N) were found at positions 26, 27, 30, and 31 in avian and swine influenza viruses.
Result: Adamantane-resistant mutations known as L26F, V27A, A30T, S31N, Table: S31N
Molecular docking of potential inhibitors for influenza H7N9.
PMID: 25861376
2015
Computational and mathematical methods in medicine
Introduction: Previously, it was observed that the Asp701Asn mutation in PB2 and the Ser31Asn mutation in hemagglutinin increased the adaptability to mammals, and the Ser31Asn mutation of M2 contributed at least partly to the resistance of antivirus drugs including amantadine and rimantadine.
Steered molecular dynamics approach for promising drugs for influenza A virus targeting M2 channel proteins.
Abstract: We have used steered molecular dynamics simulation to investigate the molecular interactions between four M2 inhibitors (amantadine, rimantadine, and two other amantadine derivatives) and the M2 protein channels of influenza A virus H5N1, including the wild type (WT) and three previously identified drug-resistant variants (G34A, S31N, and V27A).
IV mutation literature information.
PMID: 
2016
ACS infectious diseases
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