Introduction: The drugs, amantadine and rimantadine, were effective against influenza A until recently when the influenza A strains became dominated by an S31N mutation displaying drug resistance.
Result: <
Result: 6 shows that the PISEMA spectra of 5 15N-labeled leucine residues in the M2 TM domain do not change significantly in the presence (red) or absence (black) of amantadine for the S31N, V27A, and A30T mutants.
Result: In order to further investigate the binding site of amantadine in M2 channels, we prepared mutants of the AM2 TM domain corresponding to the naturally occurring drug-resistant mutations, V27S, V27A, A30T, and S31N.
Oseltamivir-resistant influenza A and B viruses pre- and postantiviral therapy in children and young adults with cancer.
PMID: 21048522
2011
The Pediatric infectious disease journal
Introduction: Resistance to the second class of anti-influenza drugs, adamantanes, results in most cases from a single serine to asparagine amino acid replacement (S31N) in the matrix M2 protein, which can interfere with the drug's ability to block M2 ion channel activity and viral replication.
Result: Susceptibility to adamantanes was tested for all oseltamivir-resistant influenza A (H3N2) viruses by sequence analysis of the M gene; all strains had an S31N mutation in the transmembrane region of the M2 protein and were therefore resistant to these drugs (data not shown).
Genotypic and phenotypic resistance of pandemic A/H1N1 influenza viruses circulating in Germany.
Abstract: In addition, analysis of 1011 pandemic A/H1N1 virus samples by a PSQ-based assay according to the WHO protocol revealed the presence of mutation S31N in the M2 protein that conferred resistance to M2 ion channel inhibitors.
Pandemic H1N1 2009 influenza virus with the H275Y oseltamivir resistance neuraminidase mutation shows a small compromise in enzyme activity and viral fitness.
PMID: 21172786
2011
The Journal of antimicrobial chemotherapy
Introduction: Pandemic influenza A/H1N1 2009 virus (pH1N1) crossed into humans carrying a well-characterized amantadine-resistance mutation, S31N, within the M2 ion channel protein, rendering the adamantane class of antiviral drug ineffective against the virus.
Nationwide molecular surveillance of pandemic H1N1 influenza A virus genomes: Canada, 2009.
Discussion: All sampled Canadian viruses encoded the A/H1N1pdm signature S31N (M2) allele that conveys antiviral resistance to Amantadine.
Influenza and other respiratory viruses in three Central American countries.
PMID: 21306576
2011
Influenza and other respiratory viruses
Result: The analyses show that all influenza B (n = 10) samples were sensitive to oseltamivir, and all influenza A/H3N2 (n = 10) samples were resistant to amantadine (mutation S31N) and sensitive to oseltamivir.
[The 2009 pandemic influenza in Russia. I. Diagnosis and molecular biological characteristics of the virus].
Abstract: All the test strains contain the S31N substitution in the M2 protein, which determines viral resistance to adamantine, and have no H275Y substitution in neuraminidase, which determines oseltamivir resistance.
Exploring the size limit of templates for inhibitors of the M2 ion channel of influenza A virus.
PMID: 21466220
2011
Journal of medicinal chemistry
Abstract: Inhibition of the wild-type (wt) M2 channel and the A/M2-S31N and A/M2-V27A mutant ion channels were measured in Xenopus oocytes using two-electrode voltage clamp (TEV) assays.
Abstract: Only the smallest analogue 8 was found to inhibit the S31N mutant ion channel.
Introduction: Amongst all the new compounds tested, 8 was the only one able to inhibit A/M2 S31N channel with an IC50 of 252 muM, slightly higher than that of Amt (IC50 = 200 muM).
Introduction: Amt-resistant mutants are frequently detected among the two currently circulating subtypes of influenza A virus, A/H3N2 and A/H1N1, with the S31N mutation being observed in more than 90% of influen
Phylogenetic analysis of an off-seasonal influenza virus A (H3N2) in Niigata, Japan, 2010.
PMID: 21617310
2011
Japanese journal of infectious diseases
Abstract: These viruses exhibited the S31N mutation in M2, which confers resistance to amantadine.
Molecular dynamics simulation directed rational design of inhibitors targeting drug-resistant mutants of influenza A virus M2.
PMID: 21744829
2011
Journal of the American Chemical Society
Abstract: However, most of the current virulent influenza A viruses carry drug-resistant mutations alongside the drug binding site, such as S31N, V27A, and L26F, etc., each of which might be dominant in a given flu season.
Introduction: L26F, S31N, and V27A are relative
Introduction: Although S31N is the substitution found in current resistant strains, in other years V27A has predominated.
Introduction: Although a variety of mutations can lead to amantadine-resistance in vitro, only three mutants, S31N, V27A and L26F, are generally observed in transmissible viruses that infect pigs, birds and humans.
IV mutation literature information.
PMID: 
2011
Biochimica et biophysica acta
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