Genetic diversity of influenza A viruses circulating in Bulgaria during the 2018-2019 winter season.
PMID: 32459617
2020
Journal of medical microbiology
Abstract: HA1 D222N substitution, associated with increased virulence, was identified in two A(H1N1)pdm09 viruses.
Method: Screening of A(H1N1)pdm09 viruses for the presence of point mutations encoding NA H275Y amino acid substitution, known to confer oseltamivir resistance, was carried out using a real-time RT-PCR assay that allowed discrimination of a single nucleotide difference between oseltamivir sensitive and resistant viruses.
Discussion: D222G/N polymorphism has been reported in recently circulati
Discussion: A(H1N1)pdm09 HA1 D222G/N/S or Q293H substitutions have been associated with cases of severe disease and fatalities earlier in the pandemic period.
Effect of the selection pressure of vaccine antibodies on evolution of H9N2 avian influenza virus in chickens.
Abstract: Only a few substitutions associated with human adaptation were observed, a remarkably low prevalence of the human adaptive substitution PB2-E627K, which is common during human infection with other H5N1 clades and a known virulence marker for avian influenza viruses during human infections.
Result: Additionally, substitutions in NS1 (N200S, G205R) as well as NS2 (T47A, M51I) proteins may result in decreased antiviral responses in the host.
Result: Although Q136L is associated with reduced sensitivity to zanamivir and oseltamivir, Q136H had no effect on sensitivity to NAI when tested in H
Antibody Neutralization of an Influenza Virus that Uses Neuraminidase for Receptor Binding.
Result: As described in the Introduction, the G147R mutation enables NA to bind receptor while retaining its catalytic receptor-cleaving activity.
Result: As expected, S364N greatly increased the resistance of the virus to HF5 neutralization (Figure 3).
Result: Based on prior work, it may be possible to generate D151N as a mixed cooperating population, but we did not attempt that here.
Result: Note that unlike the other HAs in this paper, this binding-deficient HA is H3 rather than H1:our rationale for using it is that it has been shown to completely lack receptor binding activity, whereas most characterized point mutants of HA in the receptor binding pocket (e.g., the widely used Y98F mutant) still retain a sufficient binding acti
Early treatment with baloxavir marboxil in high-risk adolescent and adult outpatients with uncomplicated influenza (CAPSTONE-2): a randomised, placebo-controlled, phase 3 trial.
PMID: 32526195
2020
The Lancet. Infectious diseases
Abstract: Polymerase acidic protein variants with Ile38Thr, Ile38Met, or Ile38Asn substitutions conferring reduced baloxavir susceptibility emerged in 15 (5%) of 290 baloxavir recipients assessed for amino acid substitutions in the virus.
Characterization of Influenza A and B Viruses Circulating in Southern China During the 2017-2018 Season.
Abstract: One of the mutations (K180N) was noted to likely alter the epitope and to potentially affect the viral antigenicity.
Result: A previous study found that the amino acid substitution N180K altered the epitope and affected the viral antigenicity.
Result: All of the A/H1N1 strains circulating during January to March, as well as the 2017-2019 vaccine strain (A/Michigan/45/2015), fell into clade 6B.1, which is defined by the HA1 amino acid substitutions S84N, S162N and I216T.
Result: Another mutation P154S in the Ca2 antigenic site was also found in two isolates (SMU214 and SMU941).
Result: Five mutations located in the HA antigenic epitopes were identified in the 19 B/Victoria isol
Identification of a Permissive Secondary Mutation That Restores the Enzymatic Activity of Oseltamivir Resistance Mutation H275Y.
Result: After 20 hours' incubation, expression of M2(S31N) reduced yeast growth to 30.6 +- 11.6% (mean +- SD) of the strain treated with glucose, while expression of M2(S31) reduced growth to 24.4 +- 12.9% of glucose-treated cells.
Result: Although not assessed by TEVC or plaque reduction assay, a thiophene derivative (compound 6) was selected as it restores growth of bacteria expressing M2(S31N), which would otherwise inhibit bacterial growth, with an EC50 of 25 microM.
Result: As expected, amantadine effectively inhibited PR8M2(S31) replication (EC50 = 0.16 +- 0.02 microM; mean +- s.e.m.) but not PR8M2(S31N) (EC50 > 5 microM), while M2WSJ352 selectively inhibited PR8M2(S31N) (EC50 = 3.2 +- 1.2 microM) over PR8M2(S31) (EC50 = 32.7 +- 16.1 mic
Pre-existing immunity to influenza virus hemagglutinin stalk might drive selection for antibody-escape mutant viruses in a human challenge model.
Method: Molecules expected to undergo steric clash upon A388V mutation were predicted using the default clash parameter in UCSF Chimera.
Method: The effect of the A388V mutation on the increase of viral resistance to three bNAbs (CR6261, CR9114 and FI6V3) was measured using wild-type (A388) and mutant (V388) H1N1pdm viruses generated by reverse genetics.
Method: To measure the effect of the A388V mutation on the HA structure, full-length wild-type or mutant HAs, produced as described above, were diluted in PBS (3 mug ml-1) and added to 96-well ELISA plates (50 mul per well) (catalog no.
Method: To show that the stalk-only A388V construct closely represents the stalk structure in the full-length A388V HA, the magnitude of the
Predominance of influenza virus A(H3N2) 3C.2a1b and A(H1N1)pdm09 6B.1A5A genetic subclades in the WHO European Region, 2018-2019.
Abstract: All genetically characterized A(H1N1)pdm09 viruses fell in subclade 6B.1A, of which 90% carried the amino acid substitution S183P in the HA gene.
Replication of a Dog-Origin H6N1 Influenza Virus in Cell Culture and Mice.
Abstract: This report verifies PB2 E627K mutation in virulence and spotlights the potential for the dog H6N1 virus to extend interspecies transmission.
Introduction: Mutations on these RNP component proteins could change the viral polymerase activity and virulence, such as PA P190S and PA Q400P in H7N3, PA T97I in H6N1, PB1 T296R in H1N1, PB2 E627K in H7N9 and PB2 Q591K in H9N2.
IV mutation literature information.
PMID: 
2020
Journal of medical microbiology
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