Influenza antiviral resistance in the Asia-Pacific region during 2011

Leang, Sook-Kwan; Deng, Yi‐Mo; Shaw, Robert; Caldwell, Natalie; Iannello, Pina; Komadina, Naomi; Buchy, Philippe; Chittaganpitch, Malinee; Dwyer, Dominic E.; Fagan, Peter K.; Gourinat, Ann-Claire; Hammill, Frances; Horwood, Paul F.; Huang, Q. Sue; Ip, Peng Kei; Jennings, Lance C.; Kesson, Alison; Kok, Tuckweng; Kool, J. L.; Levy, Avram; Cui, Lin; Lindsay, Katie; Osman, Osmali; Papadakis, Gina; Rahnamal, Fahimeh; Rawlinson, William D.; Redden, Craig; Ridgway, Jennifer; Sam, I‐Ching; Svobodová, Suzanne; Tandoc, Amado; Wickramasinghe, Geethani; Williamson, Jan; Wilson, Noelene; Yusof, Mohd Apandi; Kelso, Anne; Barr, Ian G.; Hurt, Aeron C.

doi:10.1016/j.antiviral.2012.12.016

Cited by 35 publications

(36 citation statements)

References 18 publications

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“…Misdiagnosis can have an impact on the therapies being used in patient management and may unnecessarily result in therapy being stopped, modified or inappropriately continued. In addition to the Q136K/R variants described here, there are many other NA mutations that alter NAI susceptibility and also appear to be selected during MDCK cell culture [19,23]. Interestingly these seem to be increasingly reported for influenza B viruses [23][24][25].…”

Section: Discussionmentioning

confidence: 99%

Zanamivir-resistant influenza viruses with Q136K or Q136R neuraminidase residue mutations can arise during MDCK cell culture creating challenges for antiviral susceptibility monitoring

et al. 2015

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Surveillance of circulating influenza strains for antiviral susceptibility is important to ensure patient treatment guidelines remain appropriate. Influenza A(H3N2) and A(H1N1)pdm09 virus isolates containing mutations at the Q136 residue of the neuraminidase (NA) that conferred reduced susceptibility to the NA inhibitor (NAI) zanamivir were detected during antiviral susceptibility monitoring. Interestingly, the mutations were not detectable in the viruses from respective clinical specimens, only in the cultured isolates. We showed that variant viruses containing the Q136K and Q136R NA mutations were preferentially selected in MadinDarby canine kidney epithelial (MDCK) cells, but were less well supported in MDCK-SIAT1 cells and embryonated eggs. The effect of Q136K, Q136R, Q136H and Q136L substitutions in NA subtypes N1 and N2 on NAI susceptibility and in vitro viral fitness was assessed. This study highlights the challenges that cell culture derived mutations can pose to the NAI susceptibility analysis and interpretation and reaffirms the need to sequence viruses from respective clinical specimens to avoid misdiagnosis. However, we also demonstrate that NA mutations at residue Q136 can confer reduced zanamivir, peramivir or laninamivir susceptibility, and therefore close monitoring of viruses for mutations at this site from patients being treated with these antivirals is important.

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Section: Discussionmentioning

confidence: 99%

Zanamivir-resistant influenza viruses with Q136K or Q136R neuraminidase residue mutations can arise during MDCK cell culture creating challenges for antiviral susceptibility monitoring

et al. 2015

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“…The prevalence of oseltamivir-resistant H1N1p viruses remained low worldwide in the post-pandemic period, albeit at a slight increase from their level during the pandemic period [24,25,26]. Nonetheless, the rate of oseltamivir resistance is much higher among high-risk groups such as immunocompromised patients, and clusters of high community transmission rates have been reported [25,27].…”

Section: Discussionmentioning

confidence: 99%

Characterization of Human Influenza Viruses in Lebanon during 2010-2011 and 2011-2012 Post-Pandemic Seasons

Zaraket¹,

Dapat

Ghanem

et al. 2014

Intervirology

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Objective: To genetically characterize human influenza viruses and their susceptibilities to antivirals during two post-pandemic seasons in Lebanon. Methods: Influenza virus was isolated from nasopharyngeal swabs that were obtained from patients with influenza-like illness during 2010-2012 and further analyzed both phenotypically and genotypically. Results: During the 2010-2011 season, both 2009 pandemic H1N1 (H1N1p) and B viruses co-circulated with equal prevalence, while the H3N2 virus predominated during the 2011-2012 season. All H3N2 and H1N1 viruses were resistant to amantadine. Importantly, all viruses of the influenza A and B types were susceptible to the neuraminidase (NA) inhibitors oseltamivir, zanamivir, peramivir, and laninamivir. Nonetheless, all 2011-2012 H1N1p isolates had three mutations (V241I, N369K, and N386S) in the NA gene that were suggested to be permissive of the H275Y mutation, which confers resistance to oseltamivir. We also detected one H1N1p virus during the 2010-2011 season with a 4-fold decrease in susceptibility to oseltamivir due to an NA-S247N mutation. This isolate was phylogenetically distinct from other H1N1p viruses that were isolated in other regions. Conclusions: Influenza A viruses with reduced susceptibility to oseltamivir and mutations permissive for acquiring NA resistance-conferring mutation with minimal burden on their fitness were isolated in Lebanon.

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“…Peramivir shows a cross resistance with oseltamivir to the A/H1N1 virus with H274Y mutation (Nguyen et al, 2010) which was the most concerning mutant to cause worldwide epidemic until the 2008/09 season (http://www.who.int/ influenza/resources/documents/H1N1webupdate20090318_ed_ns. pdf, WHO, last accessed April 9, 2013), where A/H1N1pdm09 with H274Y mutation had already begun to appear (Leang et al, 2013). Fortunately, the H274Y mutant is susceptible to laninamivir and zanamivir (Nguyen et al, 2010).…”

Section: Discussionmentioning

confidence: 93%

Efficacy of a single intravenous administration of laninamivir (an active metabolite of laninamivir octanoate) in an influenza virus infection mouse model

et al. 2013

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Influenza antiviral resistance in the Asia-Pacific region during 2011

Cited by 35 publications

References 18 publications

Zanamivir-resistant influenza viruses with Q136K or Q136R neuraminidase residue mutations can arise during MDCK cell culture creating challenges for antiviral susceptibility monitoring

Zanamivir-resistant influenza viruses with Q136K or Q136R neuraminidase residue mutations can arise during MDCK cell culture creating challenges for antiviral susceptibility monitoring

Characterization of Human Influenza Viruses in Lebanon during 2010-2011 and 2011-2012 Post-Pandemic Seasons

Efficacy of a single intravenous administration of laninamivir (an active metabolite of laninamivir octanoate) in an influenza virus infection mouse model

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