Influenza A(H7N9) virus acquires resistance-related neuraminidase I222T substitution when infected mallards are exposed to low levels of oseltamivir in water.
PMID: 26077257
2015
Antimicrobial agents and chemotherapy
Discussion: NA I222T and several other amino acid substitutions at the 222 NA residue generate reduced sensitivity to NAIs, either as independent resistance substitutions or, perhaps of more concern, by enhancing resistance induced by H274Y in N1 virus or by E119V in N2 virus.
Discussion: Several substitutions also seem to restore reduced fitness: I222T/V/R combined with H274Y in N1 virus and I222V combined with E119V in N2 virus.
Surveillance of antiviral resistance markers in Argentina: detection of E119V neuraminidase mutation in a post-treatment immunocompromised patient.
Abstract: RESULTS: The E119V variant was detected in only one patient during oseltamivir therapy, exhibiting decreased susceptibility to oseltamivir.
Abstract: STUDY DESIGN: We measured the populations of the low-susceptibility influenza A H3N2 variants E119V and R292K by qRT-PCR using 305 nasal aspiration samples collected over time from 13, 16, and 11 patients treated with no neuraminidase inhibitors, oseltamivir, and zanamivir, respectively.
Neuraminidase Mutations Conferring Resistance to Oseltamivir in Influenza A(H7N9) Viruses.
Abstract: Collectively, we demonstrate that R292K, E119V, and I222K reduced the inhibitory activity of oseltamivir, not only in the NI assay, but also in infected ferrets, judged particularly by viral loads in nasal washes, and may signal the need for alternative therapeutics.
Abstract: Conversely, treatment failed to significantly inhibit the replication of R292K or E119V virus.
Abstract: In the NA inhibition (NI) assay, R292K conferred highly reduced inhibition by oseltamivir, while E119V and I222K each caused reduced inhibition.
Characterization of drug-resistant influenza A(H7N9) variants isolated from an oseltamivir-treated patient in Taiwan.
PMID: 25124927
2015
The Journal of infectious diseases
Abstract: METHODS: Four NA variants of A/Taiwan/1/2013(H7N9) virus containing a single substitution (NA-E119V, NA-I222K, NA-I222R, or NA-R292K) recovered from an oseltamivir-treated patient were tested for NAI susceptibility in vitro; their replicative fitness was evaluated in cell culture, mice, and ferrets.
Abstract: RESULTS: NA-R292K led to highly reduced inhibition by oseltamivir and peramivir, while NA-E119V, NA-I222K, and <
Global update on the susceptibility of human influenza viruses to neuraminidase inhibitors, 2013-2014.
Abstract: Those showing HRI were A(H1N1)pdm09 with NA H275Y (n=169), A(H3N2) with NA E119V (n=1), B/Victoria-lineage with NA E117G (n=1) and B/Yamagata-lineage with NA H273Y (n=1); amino acid position numbering is A subtype and B type specific.
Method: In the AVWG table, it is listed that the NA E119V substitution confers 18-fold (RI) to 2057-fold (HRI) increases in oseltamivir IC50.
Method: One A(H3N2) virus from the United States contained a NA E119V substitution which conferred HRI by oseltamivir but had no effect on susceptibilit
Influenza A viruses of swine circulating in the United States during 2009-2014 are susceptible to neuraminidase inhibitors but show lineage-dependent resistance to adamantanes.
Method: (accessed 10/23/2014) were screened for the presence of known molecular markers (N2 numbering) of NAI resistance that demonstrated clinical relevance in human influenza A viruses of N1 (D198N, I222R, H274Y, N294S) or N2 (E119V, R292K, N294S) subtypes, and for NA markers reported in surveillance studies or in recombinant viruses of N1 (V116A, I117V, E119V, Q136L/K, V149A, Y155H, I222V/M/K,
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 addition, a combination of a 4-amino-acid deletion at residues 245 to 248 (Delta245-248) accompanied by the E119V substitution occurred, causing resistance to or reduced inhibition by NAIs (oseltamivir, zanamivir, and peramivir).
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: Although treatment information was unavailable for one of the cases, two of the E119V variant viruses came from patients undergoing oseltamivir treatment.
Method: The E119V and R292K substitutions were also detected in the corresponding clinical specimens.
Method: The E119V substitution conferred increases in
Characterization of drug-resistant influenza virus A(H1N1) and A(H3N2) variants selected in vitro with laninamivir.
PMID: 24957832
2014
Antimicrobial agents and chemotherapy
Abstract: More specifically, it retained activity against oseltamivir-resistant H275Y and N295S A(H1N1) variants and the E119V A(H3N2) variant.
Solid phase assay for comparing reactivation rates of neuraminidases of influenza wild type and resistant mutants after inhibitor removal.
Abstract: Viruses with H274Y, E119V and E119G mutations demonstrated faster dissociati
Result: For the H1N1 H274Y, H3N2 E119V, and clade 2 H5N1 viruses with reduced oseltamivir sensitivity, dissociation was even faster, from 12 - 16 min (p < 0.001 compared to each wild type pair).
Result: Interestingly T1/2 values were similar for the mutants, regardless of how high the IC50 was (H274Y 2440 nM, E119V 260 nM and clade 2 H5N1 19.6 nM, compared to wild type values of H1N1 3.1 nM, H3N2 5.3 nM and clade 1 H5N1 of 0.6 nM).
Result: Thus this novel assay demonstrates that there are subtle impacts on drug binding both with the H5N1 and E119V mutant not readily seen by just determining just a single IC50.
IV mutation literature information.
PMID: 
2015
Antimicrobial agents and chemotherapy
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