In the model system, oseltamivir-sensitive and resistant influenza can infect people in 321 cities connected by air travel. This model tests how oseltamivir-resistant strains would spread relative to their sensitive counterparts, and how the usage of the drug could increase the prevalence of drug-resistant influenza. Using this well developed model, the group found that a drug-resistant virus would be unable to establish itself, even if only slightly less transmissible than the sensitive virus. This explains the lack of resistance in H1N1 in the 1990s, though by 2007 seasonal H1N1 had acquired mutations that eliminated the fitness difference between sensitive and resistant strains. The model analysis showed that mutations that increased transmissibility in untreated individuals were associated with the most rapid increases in drug resistant H1N1.
These findings have implications for predicting the spread of resistance in the 2009 pandemic influenza. Increased infection control for treated individuals may slow the spread of drug-resistant strains of influenza by delaying the establishment of resistant strains in the global population. Importantly, these results show that resistant pandemic H1N1 might be slightly reduced in transmissibility, and the resistant virus would not continue to spread if it is less transmissible than the oseltamivir-sensitive counterpart.
Chao DL, Bloom JD, Kochin BF, Antia R, Longini IM. 2011. The global spread of drug-resistant influenza. Journal of the Royal Society Interface. doi: 10.1098/rsif.2011.0427