Neuraminidase sequence analysis and susceptibilities of influenza virus clinical isolates to zanamivir and oseltamivir.
PMID: 12821478
2003
Antimicrobial agents and chemotherapy
Abstract: The drug susceptibilities of known zanamivir- and oseltamivir-resistant viruses with the NA mutations E119V, R292K, H274Y, and R152K fell well outside the 95% confidence limits of the IC(50)s for all natural isolates.
A point mutation in influenza B neuraminidase confers resistance to peramivir and loss of slow binding.
Abstract: In contrast, the P15R enzyme did not display the property of slow binding and was inhibited competitively with a K(i) value of 4.69+/-0.44nM.
Abstract: Passage 15 (P15R) virus contained an additional 3 HA mutations, plus the NA mutation His273Tyr.
Abstract: The WT and P15R NAs displayed IC(50) values of 8.4+/-0.4 and 127+/-16 nM, respectively, for peramivir.
Abstract: The mechanism of inhibition of WT and P15R NA by peramivir was examined in enzyme assays.
Ser624 of the PA subunit of influenza A virus is not essential for viral growth in cells and mice, but required for the maximal viral growth.
Abstract: The LD50 of S624A virus and WSN for intranasal infection in Balb/C mice was 4.0 x 10(4) and 9.3 x 10(3) PFU, respectively.
Abstract: The growth of S624A virus was less extensive than that of WSN in cells.
Abstract: To examine the role of this protease activity in the viral infection cycle, we compared the growth and the pathogenesis of influenza A/WSN/33 (WSN) and the virus encoding a PA with a S624A mutation (S624A virus), which were generated by the plasmid-based rescue system.
A recombinant influenza A virus expressing an RNA-binding-defective NS1 protein induces high levels of beta interferon and is attenuated in mice.
Abstract: Interestingly, passaging in MDCK cells resulted in the selection of a mutant virus containing a third mutation at amino acid residue 42 of the NS1 protein (S42G).
[Key role of Asp16 in proteolysis of influenza A NP protein by caspases in infected cells].
1Abstract: To verify the above assumption the NP chimeric gene of human influenza virus was developed; Asp16 was replaced by Gly by means of ""site-oriented"" mutagenesis in the above gene, after that, the A/WSN/33 (H1N1) mutant of human influenza virus with ""avian"" NP and with point mutation (Gly16) was developed by using the method of ""reverse genetics""."
Detection of influenza virus resistance to neuraminidase inhibitors by an enzyme inhibition assay.
Abstract: addition of PO4(3-), Ca2+, DMSO, or EDTA) than wild-type enzymes or a mutant NA with an Arg292-->Lys substitution.
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.
Influenza a virus M2 ion channel activity is essential for efficient replication in tissue culture.
Abstract: N31S-M2WSN was amantadine sensitive, whereas A/WSN/33 was amantadine resistant, indicating that the M2 residue N31 is the sole determinant of resistance of A/WSN/33 to amantadine.
Abstract: We have investigated the effect of amantadine on the growth of four influenza viruses: A/WSN/33; N31S-M2WSN, a mutant in which an asparagine residue at position 31 in the M2 TM domain was replaced with a serine residue; MUd/WSN, which possesses seven RNA segments from WSN plus the RNA segment 7 derived from A/Udorn/72; and A/Udorn/72.
Use of pseudotyped retroviral vectors to analyze the receptor-binding pocket of hemagglutinin from a pathogenic avian influenza A virus (H7 subtype).
Abstract: C560Y HA was expressed nonpolarly on the surface of infected MDCK cells.
Abstract: Interestingly, viral budding remained apical in C560Y virus-infected cells, and so did the location of NP and M1 proteins at late times of infection.
Abstract: We investigated this hypothesis by infecting MDCK cells with a transfectant influenza virus carrying a mutant form of HA (C560Y) with a basolateral sorting signal in its cytoplasmic domain.
IV mutation literature information.
PMID: 
2003
Antimicrobial agents and chemotherapy
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