Abstract: The F gene segment of each of these viruses was sequenced and in each case the mutant RNA segment contained at least one sequence alteration, converting asparagine 276 to tyrosine (F1 protein).
Characterization of an influenza A (H3N2) virus resistant to the cyclopentane neuraminidase inhibitor RWJ-270201.
Abstract: Using chimeric constructs based on A/Singapore/1/57 and A/England/12/62 NAs, we localized the determinants of high specific NA activity to a region containing six amino acid substitutions in A/England/12/62: Ser331-->Arg, Asp339-->Asn, Asn367-->Ser, Ser370-->Leu, Asn400-->Ser, and Pro431-->Glu.
Comparison of the activities of zanamivir, oseltamivir, and RWJ-270201 against clinical isolates of influenza virus and neuraminidase inhibitor-resistant variants.
PMID: 11709315
2001
Antimicrobial agents and chemotherapy
Abstract: A zanamivir-resistant variant bearing a Glu119-to-Gly (Glu119-->Gly) or Glu119-->Ala substitution in an NA (N2) remained susceptible to RWJ-270201 and oseltamivir carboxylate.
Abstract: However, a zanamivir-selected variant with an Arg292-->Lys substitution in an NA (N2) showed a moderate level of resistance to RWJ-270201 (IC(50) = 30 nM) and zanamivir (IC(50) = 20 nM) and a high level of resistance to oseltamivir carboxylate (IC(50) > 3,000 nM).
Abstract: The oseltamivir-selected variant (N1) with the His274-->Tyr substitution exhibited resistance to oseltamivir carboxylate (IC(50) = 400 nM) and to RWJ-270201 (IC(50) = 40 nM) but retained full susceptibility to zanamivir (IC(50) = 1.5 nM).
Abstract: The zanamivir-resist
Host mediated variation and receptor binding specificity of influenza viruses.
PMID: 14533814
2001
Advances in experimental medicine and biology
Abstract: Only single amino acid alteration of Leu 226 to Gln made remarkable change of receptor binding specificity 2-6 to 2-3.
Abstract: When Ser 205 is substituted to Tyr, receptor binding specificity become 2-6 predominant rather than 2-3 predominant.
Differential requirement for CD80 and CD80/CD86-dependent costimulation in the lung immune response to an influenza virus infection.
PMID: 10604996
2000
Journal of immunology (Baltimore, Md.
Abstract: However, Y100F-Ig treatment had a clear effect on lung effector cell function.
Abstract: Treatment with Y100F-Ig, a mutant form of CTLA4-Ig which selectively binds to CD80 and blocks the CD28-CD80 interaction leaving CD28-CD86 binding intact, did not affect Ab production, spleen cytotoxic precursors, or clearance of virus.
Fusion protein of the paramyxovirus SV5: destabilizing and stabilizing mutants of fusion activation.
Abstract: Compared with the W3A F protein, mutant S443P enhanced the fusion kinetics with a faster rate and greater extent, and had a lower activation temperature.
Abstract: Mutant P22L did not cause fusion under physiological conditions, but fusion was activated at elevated temperatures.
Abstract: Mutant V516A had little effect on F protein-mediated fusion.
Abstract: SV5 strains W3A and WR differ by three amino acid residues at positions 22, 443, and 516.
Abstract: The double-mutant P22L,S443P was capable of causing fusion, suggesting that the two mutations have opposing effects on fusion activation.
Abstract: The fusion (F) protein of the paramyxovirus SV5 strain W3A causes sy
Influenza-associated encephalopathy in Japan: pathogenesis and treatment.
Abstract: A novel substitution at the receptor-binding site (Tyr 137 to Phe) was reported to be found exclusively in influenza type A (H3N2) viruses isolated from patients with influenza encephalopathy, suggesting that encephalopathy may be caused by a variant influenza type A (H3N2) virus.
[Variants of influenza H1N1 virus, adapted to mouse lungs and inhibitors of mouse serum inhibitors differ by hemagglutinin characteristics and structure].
Abstract: One of glycosylation site (GS) located at the tip of HA spike near the receptor binding site is lost because of mutations in both variants: GS 158 (Asn158Asp substitution) in USSR/90-MS and GS131 (Asp131Asp substitution) in USSR/90-ML.
Antigenic drift in the influenza A virus (H3N2) nucleoprotein and escape from recognition by cytotoxic T lymphocytes.
IV mutation literature information.
PMID: 
2001
Microbiology and immunology
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