Abstract: Sensitive molecular techniques are needed for rapid detection of the R292K oseltamivir-resistant mutant of influenza A(H7/N9) virus strain to monitor its transmission and guide antiviral treatment.
Introduction: Studies have shown that the NA R292K mutation can cause a high level of resistance to oseltamivir in influenza A(H7N9) virus .
Introduction: We reported emergence of an influenza virus with a mutation in the neuraminidase (NA) gene (R292K) and its association with severe clinical outcome in infected persons.
Method: Seven of 11 samples had positive results in the R292K assay: 5 samples positive in the 292K assay and 2 samples positive in both assays.
Method: The <
The R292K mutation that confers resistance to neuraminidase inhibitors leads to competitive fitness loss of A/Shanghai/1/2013 (H7N9) influenza virus in ferrets.
PMID: 24951824
2014
The Journal of infectious diseases
Abstract: An NA-R292K mutation that confers broad-spectrum resistance to NA inhibitors has been documented in H7N9 patients after treatment.
Abstract: CONCLUSIONS: The NA inhibitor-resistant H7N9 virus with the NA-R292K mutation may transmit among ferrets but showed compromised fitness in vivo while in competition with the wild-type virus.
Abstract: In ferrets inoculated with the plaque-purified A/Shanghai/1/2013 NA-R292K virus with dominant K292 (94%), the resistant K292 genotype was outgrown by the wild-type R292 genotype during the course of infection.
Abstract: METHODS: We evaluated the transmission potential of a human influenza A H7N9 isolate with
Global update on the susceptibility of human influenza viruses to neuraminidase inhibitors, 2012-2013.
Abstract: Those showing HRI were A(H1N1)pdm09 with NA H275Y (n=18), A(H3N2) with NA E119V (n=3) or NA R292K (n=1) and B/Victoria-lineage with NA H273Y (n=2); amino acid position numbering is A subtype and B type specific.
Method: An A(H3N2) virus with a R292K NA substitution was also recovered from an oseltamivir-treated patient.
Method: The E119V and R292K substitutions were also detected in the corresponding clinical specimens.
Multiple influenza A (H3N2) mutations conferring resistance to neuraminidase inhibitors in a bone marrow transplant recipient.
PMID: 25246391
2014
Antimicrobial agents and chemotherapy
Abstract: In-depth analysis by deep gene sequencing revealed that various known markers of antiviral resistance, including transient R292K and Q136K substitutions and a sustained E119K (N2 numbering) substitution in the NA protein emerged during prolonged antiviral therapy.
Drug susceptibility profile and pathogenicity of H7N9 influenza virus (Anhui1 lineage) with R292K substitution.
Discussion: The addition of exogenous NA from Clostridium perfringens greatly facilitated this process, possibly because of the low NA activity exhibited by the R292K variants.
Discussion: The compromised pathogenicity in vivo is attributed to the combined NA R292K and HA R220G mutations.
Discussion: The in vivo fitness of the R292K H7N9 variant virus should be further assessed with genetically well-characterized pairs of viruses and most desirably, with competitive fitn
Discussion: Thus, it is of clinical and scientific importance to characterize R292K variants of the dominant Anhui1 lineage (the dominant H7N9 virus lineage) from clinical specimens.
Molecular assays for quantitative and qualitative detection of influenza virus and oseltamivir resistance mutations.
PMID: 23597879
2013
The Journal of molecular diagnostics
Abstract: Four assays are included for detection of oseltamivir resistance mutations H275Y in prepandemic and pandemic influenza A/H1N1 and E119V and R292K in influenza A/H3N2 neuraminidase.
Occurrence and characterization of oseltamivir-resistant influenza virus in children between 2007-2008 and 2008-2009 seasons.
Method: For the genotypic analysis, mutations of amino acid regions related to drug resistance (E119V, R152K, H274Y, R292K, and N294S) were examined, via sequence analysis of NA gene.
Result: NA gene analysis was conducted on influenza viruses isolated from 51 patients (group A, 29 patients; group B, 22 patients) during the first study period in order to examine the drug resistance-related mutation of NA inhibitor (E119V, R152K, H274Y, R292K, N294S).
Simultaneous detection of oseltamivir- and amantadine-resistant influenza by oligonucleotide microarray visualization.
Discussion: For instance, I117V, I117M, S247N, I223R, N294S, and R292K of NA have been reported to be associated with NA inhibitor resistance, and some of them had combinatorial, compensatory, or synergistic effects.
Resistance mutation R292K is induced in influenza A(H6N2) virus by exposure of infected mallards to low levels of oseltamivir.
Method: All R292K mutants showed relatively low NA activity and were diluted 1:2 while wild type virus samples were further diluted.
Method: Sequencing of the HA gene was performed on 8 selected samples, among which 6 were evaluable, from the 12 microg/L experiment that were NA sequenced as wild type, R292K, R292K and D113N, R292K and D141N prior to and after egg propagation.
Result: At 12 microg/L of OC, the resistance mutation R292K (the arginine codon AGA changed to the lysine codon AAA) in the NA occurred in the first generation of mallards 4 days pi as a mixed genotype, and dominated from day
Generation and Characterization of Recombinant Influenza A(H1N1) Viruses Resistant to Neuraminidase Inhibitors.
PMID: 24524021
2013
Osong public health and research perspectives
Introduction: Other NA mutations (N2 numbering: E119G, H274Y, R292K, and N295S) that have been reported to confer resistance to NAIs were each introduced into recombinant A/Vietnam/1203/04(H5N1) influenza virus.
IV mutation literature information.
PMID: 
2014
Emerging infectious diseases
Browser Board
Co-occurred Entities
Filtrator
ViMRT