Abstract: For adamantanes, a high proportion (>74%) of A(H3N2) viruses had the S31N mutation in M2 protein, while variation in the HA(1) region of adamantane-sensitive viruses suggested that adamantane-sensitive variants were reseeded into the Dutch population and re-emerged as drug-sensitive due to M-segment reassortment.
Amantadine- and oseltamivir-resistant variants of influenza A viruses in Thailand.
PMID: 19850010
2009
Biochemical and biophysical research communications
Abstract: Our results demonstrated that seven out of 32 (22%) of the H1N1 viruses isolated in 2006 in Thailand carried the amino acid S31N substitution, which confers amantadine-resistance, although no isolates in 2007 or 2008 possessed the mutation.
Design and pharmacological characterization of inhibitors of amantadine-resistant mutants of the M2 ion channel of influenza A virus.
Abstract: The A/M2 proton channel of influenza A virus is a target for the anti-influenza drugs amantadine and rimantadine, whose effectiveness was diminished by the appearance of naturally occurring point mutants in the A/M2 channel pore, among which the most common are S31N, V27A, and L26F.
Result: S31N is a highly frequent mutation, which gives rise to decreased sensitivity to amantadine (IC50 = 237.0 muM versus 15.8 muM for the wt A/M2 channel, Figure 2), and complete resistance to rimantadine (IC50 > 10mM).
Table: S31N
Figure: A/M2- S31N with amantadine IC50=237.01+-22.14; with BL-1743 IC50>10 mM; with spiran amine 8 IC50>10
Detection of adamantane-resistant influenza on a microarray.
Abstract: Microarray data from a larger set of samples were further analyzed using an artificial neural network and resulted in a correct identification rate of 94% for influenza virus samples that had V27A and S31N mutations.
Abstract: STUDY DESIGN: We have taken advantage of functional genomics and microarray technology to design a DNA microarray that can detect the two most common mutations in the M2 protein associated with adamantane resistance, V27A and S31N.
[Molecular and genetic analysis of influenza A viruses isolated in Russia, based on the neuraminidase and M2 protein gene sequence].
PMID: 18488446
2008
Molekuliarnaia genetika, mikrobiologiia i virusologiia
Abstract: Besides S31N substitution, additional mutations were detected in both proteins.
Abstract: Mutations associated with S31N substitution were detected in each virus subtype, which may be considered as new markers for the identification of remantadin-resistant strains.
Abstract: The M2 sequences analysis among the remantadin resistant viruses demonstrated the S31N substitution in all strains.
Backbone structure of the amantadine-blocked trans-membrane domain M2 proton channel from Influenza A virus.
Abstract: After five sequential passages in MDCK cells, the M2 protein of viruses cultivated with amantadine alone mutated at positions V27A and S31N/I.
Amantadine resistance among porcine H1N1, H1N2, and H3N2 influenza A viruses isolated in Germany between 1981 and 2001.
Abstract: S31N and/or L27A are well-known amino acid substitutions in M2 that confer amantadine resistance.
Abstract: All resistant strains contained the AA substitutions G16E, S31N, and R77Q in the membrane protein 2 (M2).
Detection of amantadine-resistant influenza A virus strains in nursing homes by PCR-restriction fragment length polymorphism analysis with nasopharyngeal swabs.
PMID: 11773097
2002
Journal of clinical microbiology
Abstract: Thirty-one viruses (91.2%) showed a change at position 31 (serine to asparagine), three viruses (8.8%) showed a change at position 30 (alanine to threonine), and none showed a change at position 27.
Influence of amantadine resistance mutations on the pH regulatory function of the M2 protein of influenza A viruses.
Abstract: A number of amino acid substitutions, e.g., L26H, A30T, S31N and G34E reduced the activity of the M2 protein of A/chicken/Germany/34 (Rostock) and caused a substantial increase in expression of the low-pH form of HA.
Abstract: Furthermore, in double mutants the 127T mutation suppressed the attenuating effects of the A30T and S31N mutations on M2 activity.