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Published sequences do not support transfer of oseltamivir resistance mutations from avian to human influenza A virus strains

Artikel i vetenskaplig tidskrift
Författare Peter Norberg
Magnus Lindh
Sigvard Olofsson
Publicerad i Bmc Infectious Diseases
Volym 15
ISSN 1471-2334
Publiceringsår 2015
Publicerad vid Institutionen för biomedicin, avdelningen för infektionssjukdomar
Språk en
Länkar dx.doi.org/10.1186/s12879-015-0860-...
Ämnesord Influenza A, Avian influenza, Tamiflu, Oseltamivir resistance, Resistance mutations, ANTIVIRAL DRUG OSELTAMIVIR, HOMOLOGOUS RECOMBINATION, NEURAMINIDASE, INHIBITORS, EVOLUTION, TAMIFLU, ADAPTATION, FATE, Infectious Diseases
Ämneskategorier Infektionsmedicin

Sammanfattning

Background: Tamiflu (oseltamivir phosphate ester, OE) is a widely used antiviral active against influenza A virus. Its active metabolite, oseltamivir carboxylate (OC), is chemically stable and secreted into wastewater treatment plants. OC contamination of natural habitats of waterfowl might induce OC resistance in influenza viruses persistently infecting waterfowl, and lead to transfer of OC-resistance from avian to human influenza. The aim of this study was to evaluate whether such has occurred. Methods: A genomics approach including phylogenetic analysis and probability calculations for homologous recombination was applied on altogether 19,755 neuraminidase (N1 and N2) genes from virus sampled in humans and birds, with and without resistance mutations. Results: No evidence for transfer of OE resistance mutations from avian to human N genes was obtained, and events suggesting recombination between human and avian influenza virus variants could not be traced in the sequence material studied. Conclusions: The results indicate that resistance in influenza viruses infecting humans is due to the selection pressure posed by the global OE administration in humans rather than transfer from avian influenza A virus strains carrying mutations induced by environmental exposure to OC.

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