IV mutation literature information.


  Mutations in PB2 and HA enhanced pathogenicity of H4N6 avian influenza virus in mice.
 PMID: 31081750       2020       The Journal of general virology
Abstract: Although individual L331I or G453R substitutions in HA did not change the pathogenicity of BJ21 in mice, both mutations significantly enhanced virulence.
Abstract: Further studies showed that the introduction of E158K and/or E627K substitutions into PB2 significantly increased polymerase activity, which led to the enhanced replication and virulence of BJ21-MA.
Abstract: Molecular analysis of BJ21-MA identified four mutations, located in proteins PB2 (E158K and E627K) and HA (L331I and G453R, H3 numbering).


  Treatment-Emergent Influenza Variant Viruses With Reduced Baloxavir Susceptibility: Impact on Clinical and Virologic Outcomes in Uncomplicated Influenza.
 PMID: 31309975       2020       The Journal of infectious diseases
Abstract: BACKGROUND: Single-dose baloxavir rapidly reduces influenza virus titers and symptoms in patients with uncomplicated influenza, but viruses with reduced in vitro susceptibility due to amino acid substitutions at position 38 of polymerase acidic protein (PA/I38X) sometimes emerge.
Abstract: CONCLUSIONS: The emergence of viruses with PA/I38X substitutions following baloxavir treatment was associated with transient rises in infectious virus titers, prolongation of virus detectability, initial delay in symptom alleviation, and uncommonly with symptom rebound.
Abstract: Median time to sustained cessation of infectious virus detection was 192, 48, and 96 hours in the baloxavir recipients with PA/I38X


  Identification of antigenic epitopes in the haemagglutinin protein of H7 avian influenza virus.
 PMID: 31508993       2020       Avian pathology
Abstract: The epitope 103RESGSS107 was highly conserved among Eurasian lineage strains of H7 AIV, whereas three amino acid substitutions (E104R, E104K and E104G) in the epitope occurred in 98.44% of North-American lineage strains.


  Oseltamivir Resistance in Severe Influenza A(H1N1)pdm09 Pneumonia and Acute Respiratory Distress Syndrome: A French Multicenter Observational Cohort Study.
 PMID: 31538643       2020       Clinical infectious diseases
Abstract: In a multicenter cohort study including 22 oseltamivir-treated patients with influenza A(H1N1)pdm09 acute respiratory distress syndrome, prevalence of the H275Y substitution in the neuraminidase, responsible for highly reduced sensitivity to oseltamivir, was 23%.
Abstract: Patients infected with the H275Y mutant virus had higher day 28 mortality than others (80% vs 12%; P = .011).


  Baloxavir Marboxil in Japanese Pediatric Patients With Influenza: Safety and Clinical and Virologic Outcomes.
 PMID: 31538644       2020       Clinical infectious diseases
Abstract: Among patients with PA/I38T/M-substituted virus emergence, those with baseline hemagglutinin inhibition (HAI) antibody titer <40 experienced delay in time to illness alleviation (median, 85.4 vs 56.0 hours in patients with higher baseline HAI antibody titer).
Abstract: CONCLUSIONS: A single, oral dose of baloxavir marboxil was well tolerated and rapidly reduced viral titers, but the common emergence of PA/I38T/M-substituted viruses warrants consideration of alternative dosing regimens in young children.
Abstract: Emergence was associated with longer infectious virus detectability (median time, 180.0 hours) and time to illness alleviation (median, 79.6 vs 42.8 hours in patients without PA/I38T/M-substituted viruses).|m


  Genetic Characterization of a Novel Reassortant H5N6 Avian Influenza Virus Identified from a 10-Year-Old Girl.
 PMID: 31666492       2020       Japanese journal of infectious diseases
Abstract: Q226L and G228S mutations were not observed, but S128P, S137A, and T160A substitutions were identified in the receptor binding sites.
Abstract: The resistance mutation D198N in the neuraminidase (NA) protein was also identified in this strain.


  Identification of a Permissive Secondary Mutation That Restores the Enzymatic Activity of Oseltamivir Resistance Mutation H275Y.
 PMID: 31669761       2020       European journal of pharmaceutical sciences
Abstract: In this study, we identified four amantadine-resistant M2 mutants among avian and human influenza A H5N1 strains circulating between 2002 and 2019: the single S31N and V27A mutants, and the S31N/L26I and S31N/V27A double mutants.
Abstract: Three compounds 6, 7, and 15 were found to significantly block all three M2 mutants: M2-S31N, M2-S31N/L26I, and M2-S31N/V27A.
Abstract: Using r


  High genetic stability in MDCK-SIAT1 passaged human influenza viruses.
 PMID: 30241880       2019       Journal of infection and chemotherapy
Abstract: NA D151G/N changes were not seen in any of the MDCK-SIAT1 passaged A/H3N2 viruses, even in the small variants analysis conducted using deep sequencing.
Abstract: MDCK-induced amino acid (AA) mutation, such as D151G/N in the neuraminidase (NA) of influenza A/H3N2 viruses, is of concern.


  Amino Acid Residue 217 in the Hemagglutinin Glycoprotein Is a Key Mediator of Avian Influenza H7N9 Virus Antigenicity.
 PMID: 30282714       2019       Journal of virology
Abstract: The HA gene sequences of viruses recovered after the fifth passage showed that the viruses readily acquired mutations at three different amino acid positions (A125T, A151T, and L217Q).
Abstract: The analysis showed that the emergent immune escape viruses contained mutations A125T, A151T, and L217Q in the hemagglutinin (HA) glycoprotein as early as passage 5 and that these mutations persisted until passage 10.
Abstract: The results revealed that a single mutation, L217Q, in the HA of H7N9 virus led to 23- and 8-fold reductions in hemagglutination inhibition (HI) titer with ferret and chick


  Molecular epidemiology of the hemagglutinin gene of prevalent influenza virus A/H1N1/pdm09 among patient in Iran.
 PMID: 30336188       2019       Virus research
Abstract: Phylogenetic analysis of the HA genes of the A/H1N1pdm09 viruses revealed the circulation of clade 6B1, characterized by amino acid substitutions S84N, S162N and I216T, where position 162 became glycosylated.



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