Abstract
BackgroundTamiflu (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.MethodsA 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.ResultsNo 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.ConclusionsThe 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-015-0860-9) contains supplementary material, which is available to authorized users.
Highlights
Tamiflu is a widely used antiviral active against influenza A virus
It is unlikely that resistance in influenza viruses infecting humans has been transferred from avian avian influenza A virus strains carrying mutations induced by environmental exposure to oseltamivir carboxylate (OC)
Information about Human N1 strains harboring any of the I117V, E119V, D198N, I222V, N294S or I314V resistance mutations
Summary
Tamiflu (oseltamivir phosphate ester, OE) is a widely used antiviral active against influenza A virus. 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. Since influenza virus infections are persistent in waterfowl it has been postulated that presence of OC in the natural habitats of such birds could induce OC resistance among the influenza virus strains that colonize waterfowl [4,5]. This apprehension has been supported by field studies describing OC resistance mutations in influenza A virus isolated from wild birds [6], and experimentally by. Zoonotic transfer of avian influenza A virus to man occurs, mostly involving H5N1, H7N7, H7N2, H7N3, and H7N9 [10,11], this usually represents a dead end because further man-to-man transfer is rare.
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