literature

IV mutation literature information.

Profiling and characterization of influenza virus N1 strains potentially resistant to multiple neuraminidase inhibitors.

PMID: 25320319 2015 Journal of virology

Abstract: Of the nine recombinant H5N1 viruses, four variants (E119D, E119A/D/G-H274Y) also showed reduced inhibition by all of the NAIs, though their overall viral fitness was impaired in vitro and/or in vivo.

Abstract: We therefore screened a known mutation(s) that could confer multidrug resistance to the currently approved NAIs oseltamivir, zanamivir, and peramivir by assessing recombinant viruses with mutant NA-encoding genes (catalytic residues R152K and R292K, framework residues E119A/D/G, D198N, H274Y, and N294S) in the backbones of the 20

Study of oseltamivir and zanamivir resistance-related mutations in influenza viruses isolated from wild mallards in Sweden.

PMID: 24558492 2014 PloS one

Method: The literature describing NAI resistance mutations has been reviewed, whereupon nine OC (V116A, I117V, E119V, D198N, I222V, H274Y, R292K, N294S and I314V) and ten ZA (V116A, R118K, E119G/A/D, Q136K, D151E/G/N, R152K, R224K, E276D, R292K and R371K)

Mutation effects of neuraminidases and their docking with ligands: a molecular dynamics and free energy calculation study.

PMID: 24218291 2013 Journal of computer-aided molecular design

Abstract: Susceptibility of influenza virus to NA inhibitors can be reinforced by some mutations; e.g., the binding free energies of ligands with N2 subtype increase from -18.0 to -42.1 kcal mol(-1) by the E119D mutation.

Combinatorial effect of two framework mutations (E119V and I222L) in the neuraminidase active site of H3N2 influenza virus on resistance to oseltamivir.

PMID: 21422222 2011 Antimicrobial agents and chemotherapy

Abstract: Among the viruses produced, the E119D+I222L mutant virus was not able to grow without bacterial NA complementation and the D198N+I222L mutant and H274Y+I222L mutant were not stable after passages in MDCK cells.

Abstract: To look at the possibility of an increased effect on the resistance phenotype of a combination of framework mutations, known to confer resistance to oseltamivir or zanamivir, with limited effect on virus fitness, we constructed 4 viruses by reverse genetics in the A/Moscow/10/99 H3N2 background containing double mutations in their neuraminidase genes: E119D+I222L, E119V+

PMID: 20523902 2010 PLoS pathogens

Introduction: Despite a high degree of conservation of these residues, the NA substitutions identified in NA inhibitor-resistant influenza viruses isolated both in vitro and clinically tend to be NA subtype-specific: E119A/G/D/V, R292K, and N294S in the N2 and N9 subtypes and H274Y and N294S in the N1 subtype.

Discussion: E119G/A/D/V NA mutations are commonly reported to be associated with NA inhibitor resistance and were identified in influenza viruses of the N2 NA subtype.

Impact of influenza A virus neuraminidase mutations on the stability, activity, and sensibility of the neuraminidase to neuraminidase inhibitors.

PMID: 18065262 2008 Journal of clinical virology

Abstract: STUDY DESIGN: In the A/Moscow/10/99 (H3N2) virus background, viruses containing mutations in NA framework residues (E119D, R156K, W178L, S179A, D198N, I222L, E227G, H274Y, E277G, N294D, and E425G) were constructed by reverse genetics.

Abstract: The D198N and the E119D mutations decreased seriously in NA activity compared to the wild-type (>10-fold).

Mutations conferring zanamivir resistance in human influenza virus N2 neuraminidases compromise virus fitness and are not stably maintained in vitro.

PMID: 16891631 2006 The Journal of antimicrobial chemotherapy

Abstract: RESULTS: H3N2 viruses generated by reverse genetics with H274Y, R292K E119V and E119D mutations were rescued.

In vitro selection and characterization of influenza A (A/N9) virus variants resistant to a novel neuraminidase inhibitor, A-315675.

PMID: 11991966 2002 Journal of virology

Abstract: However, by passage 10 (2.56 microM A-315675), two mutations (R233K, S339P) in the HA gene appeared in addition to the E119D mutation in the NA gene, resulting in a 310-fold-lower susceptibility to A-315675.

Abstract: Sequencing of the viral population identified an E119D mutation in the NA gene, but no mutations were observed in the hemagglutinin (HA) gene.

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