Abstract
Surveillance of the antiviral susceptibility of influenza viruses in Europe revealed the emergence of influenza A(H1N1) viruses naturally resistant to the anti-neuraminidase inhibitor oseltamivir (Tamiflu) [1]. Currently, resistant viruses are most prevalent in Europe (25%) but less prevalent in the Americas (16%) or the Western Pacific region (4%) [2]. In Europe, the prevalence varies between countries, with highest levels in Norway (66.5%) and France (46.6%) [3]. These frequencies are in sharp contrast with those observed for H1N1 viruses during previous seasons (0 to <1%) [4]–[8].
Highlights
Resistance was linked to the H275Y mutation (H274Y in N2 numbering) of the N1 known to confer high level resistance to oseltamivir but not to the other antineuraminidase inhibitor, zanamivir (Relenza) [9,10,11,12]
The current frequencies of resistant H1N1 viruses are not correlated with oseltamivir usage, which suggests that selective drug pressure has not been associated with continued transmission, it may have been involved in their initial emergence
To understand the molecular basis of the apparent fitness of the resistant H1N1 viruses that emerged during the 2007–2008, season we determined the enzymatic characteristics of their neuraminidase
Summary
Y p-Values are the result of the Student’s t test between the mean of Km, Vm, or Ki of the sensitive viruses versus either the resistant ones or the pre-2007–2008 viruses. When comparing the growth characteristics in vitro on MDCK SIAT-1 cells of the resistant viruses with that of sensitive viruses from the 2007–2008 season or from previous seasons, no significant differences in growth kinetics or final virus titers were observed (Figure 1). These results indicated that, at least in vitro, the presence of the H275Y mutation did not significantly impair the fitness of the viruses, unlike what had been previously reported in the case of the A/Texas/36/ 91 virus on MDCK cells [15].
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