Discussion: For example, H275Y, which is a frequent resistance mutation, changes the orientation of E277 and alters the hydrophobic pocket of the S4 subsite, which forms interactions with the 3-pentyloxy moiety of GS4071.
Discussion: For the dual mutation I223R and H275Y, the volume of the S4 subsite is reduced because of the long side-chain of arginine and tyrosine.
Discussion: In contrast, RB19 is not affected by some drug-resistant mutations such as I223R, H275Y, and I223R/H275Y NA mutants because RB19 contains a flexible chain with a large polar moiety.
Discussion: Many mutations of NAs have been reported including E119V
Simultaneous detection of oseltamivir- and amantadine-resistant influenza by oligonucleotide microarray visualization.
Abstract: Consequently, a cost-effective oligonucleotide microarray visualization method, which was based on quantum dot-catalyzed silver deposition, was developed and evaluated for the simultaneous detection of neuraminidase H275Y and E119V; matrix protein 2 V27A and S31N mutations of influenza A (H3N2), seasonal influenza A (H1N1), and 2009 influenza A (H1N1).
Introduction: Most N1 subtypes that are resistant to oseltamivir have been associated with
Method: Moreover, microarray probes ranging from 17 to 21 nucleotides were designed to detect H275Y, E119V, V27A, and S31N mutations, respectively, of the three influenza subtypes.
Molecular and serological investigations of the Influenza A(H1N1) 2009 pandemic virus in Turkey.
PMID: 23483248
2013
Medical microbiology and immunology
Abstract: Thirteen rRT-PCR positive samples were analyzed for presence of mutations that have been associated with host range, virulence, and antiviral resistance: substitution D222G in the HA, E627K in the PB2, and H275Y in the neuraminidase (NA).
Molecular characterization of influenza A(H1N1)pdm09 virus circulating during the 2009 outbreak in Thua Thien Hue, Vietnam.
PMID: 23493002
2013
Journal of infection in developing countries
Abstract: The NA amino acid substitutions identified did not include the oseltamivir-resistant H275Y substitution.
Neuraminidase inhibitor susceptibility surveillance of influenza viruses circulating worldwide during the 2011 Southern Hemisphere season.
PMID: 23575174
2013
Influenza and other respiratory viruses
Abstract: RESULTS: Influenza A(H1N1)pdm09 viruses (n = 326) were sensitive to all NAIs, except for two (0.6%) with H275Y (N1 numbering; H274Y in N2 numbering) substitution, which exhibited elevated IC50 s for oseltamivir and peramivir, and a third with previously unreported N325K substitution, exhibiting reduced susceptibility to oseltamivir.
Introduction: In September 2011, a cluster of 29 cases infected with oseltamivir-resistant influenza A(H1N1)pdm09 viruses was reported in Australia.18, 19 These oseltamivir-resistant H275Y viruses were in circulation between May, 2011, and August, 2011, a period corresponding to the peak of the SH 2011 influenza season.20 Majority of the patients from whom they were recovered had no known oseltamivir exposure.
Introduction: Resistance to NAI
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.
Abstract: However, phenotypic analysis of the virus revealed a high oseltamivir IC50 range and that H275Y substitution of the neuraminidase (NA) gene and partial variation of the hemagglutinin (HA) gene did not affect its antigenicity to the HA vaccine even though group A had a shorter hospitalization duration and fewer lower respiratory tract complications than group B.
Discussion: However, phenotypic analysis showed that oseltamivir IC50 ranged within high-level drug resistance, H275Y of NA gene and partial variation of HA gene does not affect antigenicity to HA vaccine, even though oseltamivir treatment group had shorter admisson duration
Prolonged influenza virus shedding and emergence of antiviral resistance in immunocompromised patients and ferrets.
Result: Emergence of oseltamivir resistance was studied in the animals infected with wild type virus (groups 1, 2 and 3) using an RT-PCR assay specifically detecting the H275Y oseltamivir resistance mutation (Figure 4).
Result: From day 8 onward, the H275Y mutation emerged in the virus population of all oseltamivir treated animals in both the nose and throat.
Result: In 5 (7%) of the immunocompromised patients with an influenza pH1N1 virus infection the oseltamivir resistance mutation H275Y in the neuraminidase was detected by RT-PCR during oseltamivir mono or oseltamivir/zanamivir combination therapy.
Result: The animals of groups 1, 2 and 3 had been inoculated with oseltamivir sensitive (wild type; H275) and the animals in groups 4, 5 and 6 with oseltamivir resistant vi
Virological self-sampling to monitor influenza antiviral susceptibility in a community cohort.
PMID: 23759670
2013
The Journal of antimicrobial chemotherapy
Abstract: Influenza A(H1N1)pdm09 RT-PCR-positive samples were screened for the oseltamivir resistance-inducing H275Y substitution, and a subset of samples also underwent phenotypic antiviral susceptibility testing by enzyme inhibition assay.
Abstract: No reduction in phenotypic susceptibility to neuraminidase inhibitors was detected, but five cases with minority quasi-species of oseltamivir-resistant virus (an H275Y amino acid substitution in neuraminidase) were detected.
Method: Influenza A(H1N1)pdm09-positive specimens were screened by pyrosequencing for the H275Y mutation (a CAC to TAC nucleotide substitution) in the viral neuraminidase.
Result: Screening for this H275Y
Table: H275Y
Oseltamivir-resistant influenza A(H1N1)pdm09 virus in southern Brazil.
PMID: 23778667
2013
Memorias do Instituto Oswaldo Cruz
Abstract: Clinical samples were collected in the state of Rio Grande do Sul (RS) from 2009-2011 and two NA inhibitor-resistant mutants were identified, one in 2009 (H275Y) and the other in 2011 (S247N).
IV mutation literature information.
PMID: 
2013
PloS one
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