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 IV mutation literature information.


  Monoclonal antibodies differentially affect the interaction between the hemagglutinin of H9 influenza virus escape mutants and sialic receptors.
 PMID: 15476872       2004       Virology
Abstract: A mutant virus with a L226Q substitution showed an increased affinity for the Neu5Acalpha2-3Galbeta1-4Glc.
Abstract: Several escape mutants viruses carrying the mutation N193D bound to Neu5Acalpha2-6Galbeta1-4GlcNAc considerably stronger than to Neu5Acalpha2-6Galbeta1-4Glc.


  Influence of acylation sites of influenza B virus hemagglutinin on fusion pore formation and dilation.
 PMID: 15479794       2004       Journal of virology
Abstract: However, one of the single-acylation-site mutants, C6, in which Cys581 is replaced with serine, promoted hemifusion but not pore formation.


  Role of protein kinase C betaII in influenza virus entry via late endosomes.
 PMID: 12477851       2003       Journal of virology
Abstract: Cells expressing a phosphorylation-deficient form of PKCbetaII (T500V), but not an equivalent mutant form of PKCalpha, inhibited successful influenza virus entry-with the virus accumulating in late endosomes.
Abstract: PKCbetaII T500V expression specifically blocked EGF receptor trafficking and degradation, without affecting transferrin receptor recycling.
Abstract: SFV, however, believed to enter cells from the early endosome, was unaffected by PKCbetaII T500V expression.


  Differences in conductance of M2 proton channels of two influenza viruses at low and high pH.
 PMID: 12527729       2003       The Journal of physiology
Abstract: All intermediate mutants possessed one or other property and transformation of the WM2 phenotype into that of RM2 required substitution in all three residues V27I, F38L and D44N; single substitutions in RM2 effected the opposite phenotypic change.


  Evaluation of neuraminidase enzyme assays using different substrates to measure susceptibility of influenza virus clinical isolates to neuraminidase inhibitors: report of the neuraminidase inhibitor susceptibility network.
 PMID: 12574276       2003       Journal of clinical microbiology
Abstract: Mixing experiments, whereby increasing fractions (0, 20, 40, 60, 80, and 100%) of NA from a known NI-resistant virus were mixed with the corresponding NI-sensitive parental NA, indicated that the resolution of IC(50) values was clearer with the CL assay than with FA-2 for two of the resistant variants (R152K and E119V).
Abstract: We evaluated three NA inhibition assays against a panel of five clinical isolates each of influenza virus A/H1N1, A/H3N2, and B strains and four viruses with a defined resistance genotype (R292K, H274Y, R152K, and E119V).


  A single amino acid mutation in the PA subunit of the influenza virus RNA polymerase promotes the generation of defective interfering RNAs.
 PMID: 12663810       2003       Journal of virology
1Abstract: We propose that R638A is an ""elongation"" mutant that destabilizes PA-RNA template interactions during elongation."
Abstract: A C453R mutation in PA can compensate for this defect, suggesting that amino acids C453 and R638 form part of the same domain.
Abstract: An R638A mutation of the polymerase acidic protein (PA) subunit of the RNA polymerase of influenza A/WSN/33 virus results in severe attenuation of viral growth in cell culture by promoting the synthesis of defective interfering RNAs.


  Mutations in the N-terminal region of influenza virus PB2 protein affect virus RNA replication but not transcription.
 PMID: 12692212       2003       Journal of virology
Abstract: Some of the mutations (F130Y, R142A, and R142K) were rescued into infectious virus.
Abstract: The results indicated that the W49A, F130A, and R142A mutations of PB2 reduced or abolished the capacity of mutant RNPs to synthesize RNA in vivo but did not substantially alter their ability to transcribe or carry out cap snatching in vitro.
Abstract: While the F130Y mutant virus replicated faster than the wild type, mutant viruses R142A and R142K showed a delayed accumulation of cRNA and viral RNA during the infection cycle but normal kinetics of primary transcription, as determined by the acc


  Threonine 157 of influenza virus PA polymerase subunit modulates RNA replication in infectious viruses.
 PMID: 12719592       2003       Journal of virology
Abstract: Finally, recombinant viruses with a T157E mutation in PA protein, which resulted in a drastic reduction of protease and replication activities of RNPs, were not viable.
Abstract: Viruses with a T157A mutation, which presented a severe decrease in protease activity and replication of RNPs, showed a complex phenotype: (i) transport to the nucleus of PAT157A protein was delayed, (ii) virus multiplication was reduced at both low and high multiplicities, (iii) transcriptive synthesis was unaltered while replicative synthesis, especially cRNA, was diminished, and (iv) viral pathogenesis in mice was reduced, as measured by loss of body weight and virus titers in lungs.
Abstract: Viruses with a T162A mutation, which showed a very moder


  X-ray structure of the hemagglutinin of a potential H3 avian progenitor of the 1968 Hong Kong pandemic influenza virus.
 PMID: 12758169       2003       Virology
Abstract: We find that structurally significant differences between the avian and the human HAs are restricted to the receptor-binding site particularly the substitutions Q226L and G228S that cause the site to open and residues within it to rearrange, including the conserved residues Y98, W153, and H183.


  Basic residues of the helix six domain of influenza virus M1 involved in nuclear translocation of M1 can be replaced by PTAP and YPDL late assembly domain motifs.
 PMID: 12768027       2003       Journal of virology
Abstract: Among the rescued mutant viruses, R101A and R105K exhibited reduced growth and small-plaque morphology, and all other mutant viruses showed the wild-type phenotype.
Abstract: Deletion (Delta YRKL) or mutation (4A) of YRKL also abolished generation of infectious virus.
Abstract: Furthermore, mutant M1 proteins (R101A/K102A, Delta YRKL, 4A, PTAP, 4A+PTAP, and YPDL) when expressed alone from cloned cDNAs were only cytoplasmic, whereas the wild-type M1 expressed alone was both nuclear and cytoplasmic as expected.



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