Identification of a human influenza type B strain with reduced sensitivity to neuraminidase inhibitor drugs

Hurt, Aeron C.; McKimm-Breschkin, Jennifer L.; McDonald, M.; Barr, Ian G.; Komadina, Naomi; Hampson, Alan W.

doi:10.1016/j.virusres.2004.02.035

Cited by 27 publications

(9 citation statements)

References 21 publications

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“…22 Fluorometric determinations were quantified with a Synergy 2 multimode microplate reader (BioTek, Winooski, VT, USA) and were based on the release of the fluorescent product 4-methyl-umbelliferone using excitation and emission wavelengths of 360 and 460 nm, respectively. The concentration of NAI that reduced NA activity by 50% (IC 50 ), relative to a control mixture with no NAI, was determined by plotting the percent inhibition of NA activity as a function of the compound concentrations calculated using GraphPad Prism 5 software (GraphPad Software, La Jolla, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Assessing the fitness of distinct clades of influenza A (H9N2) viruses

Schultz‐Cherry¹,

Thomas²

2013

Emerging Microbes & Infections

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Influenza A (H9N2) viruses are a genetically diverse population that infects wild and domestic avian species and mammals and contributed the internal gene segments to the A/H5N1 and A/H7N9 viruses associated with lethal human infections. Here we comprehensively assess the potential risk to mammals of a diverse panel of A/H9N2 viruses, representing the major H9N2 clades, using a combination of in vitro assays (e.g., antiviral susceptibility and virus growth in primary differentiated human airway cells) and in vivo assays (e.g., replication, transmission and/or pathogenicity of viruses in ducks, pigs, mice and ferrets). We observed that viruses isolated from humans, A/Hong Kong/1073/1999 and A/Hong Kong/33982/2009, had the highest risk potential. However, the A/swine/Hong Kong/9A-1/1998 and A/chicken/Hong Kong/G9/1997 viruses also displayed several features suggesting a fitness profile adapted to human infection and transmission. The North American avian H9N2 clade virus had the lowest risk profile, and the other viruses tested displayed various levels of fitness across individual assays. In many cases, the known genotypic polymorphisms alone were not sufficient to accurately predict the virus' phenotype. Therefore, we conclude that comprehensive risk analyses based on surveillance of circulating influenza virus strains are necessary to assess the potential for human infection by emerging influenza A viruses.

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Section: Methodsmentioning

confidence: 99%

Assessing the fitness of distinct clades of influenza A (H9N2) viruses

Schultz‐Cherry¹,

Thomas²

2013

Emerging Microbes & Infections

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“…Hurt and colleagues reported detection of an influenza B/Perth/211/2001 virus among 126 influenza B viruses (0.8%) isolated between 1998 and 2002 from Australasia and the Asia-Pacific region (Hurt et al, 2004b). The virus was isolated from an 8-month-old girl with acute respiratory illness and no history of treatment or close contact with patients under treatment with either zanamivir or oseltamivir (Hurt et al, 2006).…”

Section: Nai Resistance Among Influenza B Virusesmentioning

confidence: 99%

“…A variation of this mutation was found in one other surveillance sample, D198Y in B/Lyon CHU/8.614/2006 (Escuret et al, 2008). The D198Y NA mutation resulted in 14-fold reduction in susceptibility to both oseltamivir and zanamivir while the D198E NA mutation of B/Texas/38/2008 conferred only slight 4-14- and 2-3-fold reductions in susceptibility to oseltamivir and zanamivir, respectively (Escuret et al, 2008; Hurt et al, 2004b; Okomo-Adhiambo et al, 2010). …”

Section: Nai Resistance Among Influenza B Virusesmentioning

confidence: 99%

Neuraminidase inhibitors for influenza B virus infection: Efficacy and resistance

2013

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Many aspects of the biology and epidemiology of influenza B viruses are far less studied than for influenza A viruses, and one of these aspects is effectiveness and resistance to the clinically available antiviral drugs, the neuraminidase (NA) inhibitors (NAIs). Acute respiratory infections are one of the leading causes of death in children and adults, and influenza is among the few respiratory infections that can be prevented and treated by vaccination and antiviral treatment. Recent data has suggested that influenza B virus infections are of specific concern to pediatric patients because of the increased risk of severe disease. Treatment of influenza B is a challenging task for the following reasons: NAIs (e.g., oseltamivir and zanamivir) are the only FDA-approved class of antivirals available for treatment;the data suggest that oseltamivir is less effective than zanamivir in pediatric patients;zanamivir is not prescribed to patients younger than 7;influenza B viruses are less susceptible than influenza A viruses to NAIs in vitro;although the level of resistance to NAIs is low, the number of different molecular markers of resistance is higher than for influenza A viruses, and they are not well defined;the relationship between levels of NAI phenotypic resistance and known molecular markers, frequency of emergence, transmissibility, and fitness of NAI-resistant variants are not well established. This review presents current knowledge of the effectiveness of NAIs for influenza B virus and antiviral resistance in clinical, surveillance, and experimental studies.

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“…Furthermore, in clinical studies, changes conferring either resistance or reduced susceptibility to NAIs have been identified in the neuraminidase (NA) of influenza B viruses isolated from patients after treatment ( 3 – 6 ). Although the use of an antiviral agent can lead to the development of drug resistance, influenza B viruses with a reduced NAI susceptibility have also been recovered from patients with no history of exposure ( 5 , 7 – 10 ). It is therefore plausible that such mutations may be naturally occurring within the NA of influenza B viruses.…”

mentioning

confidence: 99%