Virusliterature

IV mutation literature information.

[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.

Mechanism of influenza A virus NS1 protein interaction with the p85beta, but not the p85alpha, subunit of phosphatidylinositol 3-kinase (PI3K) and up-regulation of PI3K activity.

PMID: 18534979 2008 The Journal of biological chemistry

Abstract: In reciprocal gain of function experiments with p85alpha, we demonstrated that mutation to Val at Met-582 leads to NS1 binding and increased PI3K activity.

Ab initio fragment molecular orbital studies of influenza virus hemagglutinin-sialosaccharide complexes toward chemical clarification about the virus host range determination.

PMID: 18574690 2008 Glycoconjugate journal

Abstract: In the ab initio FMO studies, binding energy of avian Gln226Leu H3-human alpha2-6 was quite similar to that in the human H3-human alpha2-6 complex with amino acid sequence differences at nine positions in the models.

Abstract: Opposite mutation Leu226Gln in the human H3 gave the moderate binding energies to avian alpha2-3 with similarity to avian H3-alpha2-3 complex that supported our previous virus-sialoside binding assay.

Abstract: This similarity indicates that avian Gln226Leu H3 virus can infect human with the same level as human H3 virus.

Another look at the molecular mechanism of the resistance of H5N1 influenza A virus neuraminidase (NA) to oseltamivir (OTV).

PMID: 18584938 2008 Biophysical chemistry

Abstract: In contrast to the binding free energies, the net charges of Glu276 and Arg224, making charge-charge interactions with Glu276, were established to be more sensitive to detecting subtle conformational differences induced at the key residue Glu276 by the His274X mutations.

Abstract: The smaller side chain residue mutations of His274 resulted in slightly enhanced or unchanged NA sensitivity to OTV, while His274Phe and His274Tyr reduced the susceptibility of OTV to N1.

Treatment of influenza A (H1N1) virus infections in mice and ferrets with cyanovirin-N.

PMID: 18601954 2008 Antiviral research

Abstract: Recently we created a hybrid (reassortant) influenza A/WSN/33 (H1N1) virus containing the HA gene of A/New Caledonia/20/99 (H1N1) with an Asp225Gly mutation in the HA1, that was lethal to mice yet retained sensitivity to CV-N.

Introduction: In this case the HA gene of A/New Caledonia/20/99 was genetically altered to contain an Asp225Gly mutation in the HA1 subunit.

Introduction: The Asp225Gly substitution is a mutation that effects the receptor binding site for the HA1

Result: Mice infected with the influenza A/WSN/33 HAnc-Asp225Gly (H1N1) virus were treated with doses of CV-N starting 4 h prior to virus exposure (Table 1).

A broad spectrum, one-step reverse-transcription PCR amplification of the neuraminidase gene from multiple subtypes of influenza A virus.

PMID: 18613963 2008 Virology journal

Abstract: The RT-PCR fragment generated includes one of the mutation sites related to oseltamivir resistance, H274Y.

Result: There are other residues that confer resistance to the NA inhibitors, but for the purpose of this study we focused on the H274Y mutation (an NA mutation that appears to be increasing significantly in frequency and distribution).

Result: virus subtype N1: amino acid H274Y).

Surveillance for neuraminidase inhibitor resistance among human influenza A and B viruses circulating worldwide from 2004 to 2008.

PMID: 18625765 2008 Antimicrobial agents and chemotherapy

Abstract: A rise in the incidence of oseltamivir resistance in A(H1N1) viruses carrying the H274Y mutation was detected in the United States and in other countries in the ongoing 2007 to 2008 season.

Abstract: Molecular markers of oseltamivir resistance were found in six A(H1N1) viruses (H274Y) and one A(H3N2) virus (E119V) collected between 2004 and 2007.

Abstract: Some outliers contained previously reported mutations (e.g., I222T in the B viruses), while other mutations [e.g., R371K and H274Y in B viruses and H274N in A(H3N2) viruses) were novel.

Abstract: The R371K B virus outlier exhibited high levels of resistance to both inhibitors (>100 nM).

Functional studies indicate amantadine binds to the pore of the influenza A virus M2 proton-selective ion channel.

PMID: 18669647 2008 Proc Natl Acad Sci U S A

Abstract: However, the D44A channel was found to be sensitive to amantadine when measured by electrophysiological recordings in oocytes of Xenopus laevis and in mammalian cells, and when the D44 and R45 mutations were introduced into the influenza virus genome.

Oseltamivir-resistant influenza A viruses are transmitted efficiently among guinea pigs by direct contact but not by aerosol.

PMID: 18684820 2008 Journal of virology

Abstract: Here, we demonstrate that recombinant human influenza A/H3N2 viruses without and with oseltamivir resistance mutations (in which NA carries the mutation E119V or the double mutations E119V I222V) have similar in ovo growth kinetics and infectivity in guinea pigs.

Mutations at alternative 5' splice sites of M1 mRNA negatively affect influenza A virus viability and growth rate.

PMID: 18768984 2008 Journal of virology

Abstract: More M2 mRNA was produced in G11C mutant virus-infected cells than in wild-type-virus-infected cells, and there was little M2 mRNA and none at all in G145A and G52C mutant virus-infected ones, respectively.

Abstract: On the other hand, mutants with the mutation G11C (at the 3' end of exon of the mRNA3 5' splice site), G52C (for the first nucleotide of the intron for M2 mRNA), or G145A (at the 3' end of the exon of mRNA4) were rescued, although they had significantly attenuated growth rates.

Abstract: Six different mutations at the splice sites were introduced, and viral growth characteristics for those mutants generated by reverse genetics with 12 plasmids were e

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