Dataset Information

Reversion of influenza A (H3N2) virus from amantadine resistant to amantadine sensitive by further reassortment in Japan during the 2006-to-2007 influenza season.

ABSTRACT: In the 2006-to-2007 influenza season, amantadine-sensitive strains were found among the N-lineage influenza A (H3N2) viruses, which were previously believed to be associated with amantadine resistance. Whole-genome sequencing results indicated that this was due to a further reassortment event.

SUBMITTER: Furuse Y

PROVIDER: S-EPMC2650930 | biostudies-literature | 2009 Mar

REPOSITORIES: biostudies-literature

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Reversion of influenza A (H3N2) virus from amantadine resistant to amantadine sensitive by further reassortment in Japan during the 2006-to-2007 influenza season.

Furuse Yuki Y Suzuki Akira A Kamigaki Taro T Shimizu Midori M Fuji Naoko N Oshitani Hitoshi H

Journal of clinical microbiology 20081224 3

In the 2006-to-2007 influenza season, amantadine-sensitive strains were found among the N-lineage influenza A (H3N2) viruses, which were previously believed to be associated with amantadine resistance. Whole-genome sequencing results indicated that this was due to a further reassortment event. ...[more]

PMID: 19109467

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Project description:BackgroundDuring the 2017-18 influenza season in the USA, there was a high incidence of influenza illness and mortality. However, no apparent antigenic change was identified in the dominant H3N2 viruses, and the severity of the season could not be solely attributed to a vaccine mismatch. We aimed to investigate whether the altered virus properties resulting from gene reassortment were underlying causes of the increased case number and disease severity associated with the 2017-18 influenza season.MethodsSamples included were collected from patients with influenza who were prospectively recruited during the 2016-17 and 2017-18 influenza seasons at the Johns Hopkins Hospital Emergency Departments in Baltimore, MD, USA, as well as from archived samples from Johns Hopkins Health System sites. Among 647 recruited patients with influenza A virus infection, 411 patients with whole-genome sequences were available in the Johns Hopkins Center of Excellence for Influenza Research and Surveillance network during the 2016-17 and 2017-18 seasons. Phylogenetic trees were constructed based on viral whole-genome sequences. Representative viral isolates of the two seasons were characterised in immortalised cell lines and human nasal epithelial cell cultures, and patients' demographic data and clinical outcomes were analysed.FindingsUnique H3N2 reassortment events were observed, resulting in two predominant strains in the 2017-18 season: HA clade 3C.2a2 and clade 3C.3a, which had novel gene segment constellations containing gene segments from HA clade 3C.2a1 viruses. The reassortant re3C.2a2 viruses replicated with faster kinetics and to a higher peak titre compared with the parental 3C.2a2 and 3C.2a1 viruses (48 h vs 72 h). Furthermore, patients infected with reassortant 3C.2a2 viruses had higher Influenza Severity Scores than patients infected with the parental 3C.2a2 viruses (median 3·00 [IQR 1·00-4·00] vs 1·50 [1·00-2·00]; p=0·018).InterpretationOur findings suggest that the increased severity of the 2017-18 influenza season was due in part to two intrasubtypes, cocirculating H3N2 reassortant viruses with fitness advantages over the parental viruses. This information could help inform future vaccine development and public health policies.FundingThe Center of Excellence for Influenza Research and Response in the US, National Science and Technology Council, and Chang Gung Memorial Hospital in Taiwan.

Dataset Information

Reversion of influenza A (H3N2) virus from amantadine resistant to amantadine sensitive by further reassortment in Japan during the 2006-to-2007 influenza season.

Publications

Reversion of influenza A (H3N2) virus from amantadine resistant to amantadine sensitive by further reassortment in Japan during the 2006-to-2007 influenza season.

Similar Datasets

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