Mutations of neuraminidase implicated in neuraminidase inhibitors resistance

Ferraris, Olivier; Lina, Bruno

doi:10.1016/j.jcv.2007.10.020

Cited by 153 publications

(132 citation statements)

References 56 publications

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“…Currently, an avian H5N1 virus, which emerged in May 1997, is a threat (Claas et al, 1998;Subbarao et al, 1998) and was reported to have caused almost 250 human deaths up to 2009(World Health Organization, 2004. Due to the high mutation rate and emerging resistance against neuraminidase inhibitors (Ferraris & Lina, 2008) and amantadine/rimantadine (Rahman et al, 2008), it is of utmost importance to investigate viral proteins as potential drug targets.…”

Section: Introductionmentioning

confidence: 99%

Large-scale analysis of influenza A virus sequences reveals potential drug target sites of non-structural proteins

Darapaneni

Prabhaker

Kukol

2009

Journal of General Virology

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Section: Introductionmentioning

confidence: 99%

Large-scale analysis of influenza A virus sequences reveals potential drug target sites of non-structural proteins

Darapaneni

Prabhaker

Kukol

2009

Journal of General Virology

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“…The viruses can avoid the mechanism of action such drug as inhibitors of viral proteases action after a few replication cycles [27,37].…”

Section: Resultsmentioning

confidence: 99%

Levels of Antiviral Therapy

Ap¹,

Turmagambetova²,

Berezin³

2016

JHVRV

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“…Vir al strains exhibit resistance to NA inhibitors mai nly because of amino acid mutations in conserved sites around an NA substrate-binding pocket (Ferraris and Lina, 2008). These mutations in conserved residues likely impair NA activity, thereby preventing HA-NA pseudoviruses to be generated (Zhang et al, 2010).…”

Section: Sui Tability Of H5n1 Na Pseudoviruses For Drug-resistance Asmentioning

confidence: 99%

Pseudovirus-based neuraminidase inhibition assays reveal potential H5N1 drug-resistant mutations

Jiang

2013

Protein Cell

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T he use of antiviral drugs such as influenza neuraminidase (NA) inhibitors is a critical strategy to prevent and control fl u pandemic, but this strategy faces the challenge of emerging drug-resistant strains. F or a highly pathogenic avian infl uenza (HPAI) H5N1 virus, biosafety restrictions have significantly limited the efforts to monitor its drug responses and mechanisms involved. In this study, a rapid and biosafe assay based on NA pseudovirus was developed to study the resistance of HPAI H5N1 virus to NA inhibitor drugs. The H5N1 NA pseudovirus was comprehensively tested using oseltamivir-sensitive strains and their resistant mutants. Results were consistent with those in previous studies, in which live H5N1 viruses were used. Several oseltamivir-resistant mutations reported in human H1N1 were also identifi ed to cause decreased oseltamivir sensitivity in H5N1 NA by using the H5N1 NA pseudovirus. Thus, H5N1 NA pseudoviruses could be used to monitor HPAI H5N1 drug resistance rapidly and safely.

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Mutations of neuraminidase implicated in neuraminidase inhibitors resistance

Cited by 153 publications

References 56 publications

Large-scale analysis of influenza A virus sequences reveals potential drug target sites of non-structural proteins

Large-scale analysis of influenza A virus sequences reveals potential drug target sites of non-structural proteins

Levels of Antiviral Therapy

Pseudovirus-based neuraminidase inhibition assays reveal potential H5N1 drug-resistant mutations

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