literature

IV mutation literature information.

Exploring organosilane amines as potent inhibitors and structural probes of influenza a virus M2 proton channel.

PMID: 21819109 2011 Journal of the American Chemical Society

Introduction: A/M2 is more conserved than other drug targets of influenza A virus with only three predominant drug resistant mutations S31N, V27A and L26F observed in widely circulating viruses, all of which are located in the transmembrane domain drug binding site.

Virological surveillance and antiviral resistance of human influenza virus in Argentina, 2005-2008.

PMID: 22358415 2011 Revista panamericana de salud publica

Abstract: RESULTS: Resistance to amantadine was observed only on A(H3N2) strains (29/33); all of them carried the mutation S31N in their M2 sequence.

Rapid quantification of single-nucleotide mutations in mixed influenza A viral populations using allele-specific mixture analysis.

PMID: 19761797 2010 Journal of virological methods

Abstract: The FluASMA assays target L26F, V27A, A30T, and S31N mutations in the A/Albany/1/98 (H3N2) M2 gene and H275Y mutation in the A/New Caledonia/20/99 (H1N1) NA gene and have a limit of quantification of 0.25-0.50% mutant.

Rapid and specific detection of amantadine-resistant influenza A viruses with a Ser31Asn mutation by the cycling probe method.

PMID: 19889895 2010 Journal of clinical microbiology

Abstract: In the present study, we developed a novel method to detect amantadine-resistant strains harboring the Ser31Asn mutation in the M2 gene based on the cycling probe method and real-time PCR.

Oseltamivir-resistant pandemic (H1N1)2009 in Yemen - case report.

PMID: 20459681 2010 Virology journal

Abstract: Both clinical specimens presented the mutation S31N in the M2 gene associated with resistance to adamantanes and H274Y in NA gene associated with resistance to oseltamivir.

Conclusion: Both clinical specimens presented the mutation S31N in the M2 gene associated with resistance to adamantanes.

Discussion: Moreover, this isolate, and others collected over the summer in Hong Kong have a clade 2C HA and M2 which has H274Y in NA (both clade 2B and clade C) as well as S31N on M2, signaling additional exchanges of polymorphisms6 leading to the emergence of H1N1

In vitro system for modeling influenza A virus resistance under drug pressure.

PMID: 20498316 2010 Antimicrobial agents and chemotherapy

Abstract: Sequencing of the M2 gene revealed that mutations appeared at between 48 and 72 h of drug treatment and that the mutations were identical to those identified in the clinic for amantadine-resistant viruses (e.g., V27A, A30T, and S31N).

[Detection of molecular markers of amantadine resistance in swine influenza viruses by pyrosequencing].

PMID: 20499646 2010 Wei sheng wu xue bao

Abstract: RESULTS: All 5 H1N1 swine influenza viruses were adamantine resistance, three mutations were founded in these isolates, namely V27T, V27I and S31N.

How does influenza virus a escape from amantadine?

PMID: 20521806 2010 The journal of physical chemistry. B

Abstract: Failure of channel blocking would cause AMT drug resistance in the S31N mutant.

Abstract: Mutation experiments indicate that the trans-membrane domain of M2 protein plays an essential role in AMT resistance, especially the S31N mutation.

Abstract: To investigate the details of structure and mechanism, molecular dynamics (MD) simulations and quantum mechanics/molecular mechanics (QM/MM) calculations have been carried out on both the wild-type protein and its S31N mutant.

Coexistence of two adamantane binding sites in the influenza A M2 ion channel.

PMID: 20643947 2010 Proc Natl Acad Sci U S A

Abstract: Furthermore, by examining drug binding to M2 mutant constructs (V27A, S31N, and D44A), it was possible to probe the location of the two binding sites.

Oseltamivir-resistant pandemic A/H1N1 virus is as virulent as its wild-type counterpart in mice and ferrets.

PMID: 20661429 2010 PLoS pathogens

Introduction: Early reports demonstrated that pH1N1 strains were resistant to the adamantanes due to a S31N mutation in the M2 gene but remained susceptible to neuraminidase inhibitors (NAIs) such as oseltamivir and zanamivir.

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