Abstract
Background: The recent worldwide emergence of increasing oseltamivir resistance to influenza A H1N1 may have important implications for influenza prevention and control. Objectives: To assess oseltamivir use, the emergence of resistance and the outcome of an influenza A H3N2 outbreak. Patients/Methods: Following identification of an influenza outbreak through active surveillance, the investigators offered treatment and prophylaxis with oseltamivir to both Aged Care Facility (ACF) residents and staff. The investigators conducted genotypic sensitivity testing using sequencing and rolling circle amplfication for known oseltamivir resistance mutations. Results: An influenza A H3N2 outbreak affecting an ACF with 90 residents and 79 staff was identified 6 days after the initial case. Oseltamivir prophylaxis was commenced on day 7. The overall attack rate was 10%, with 13 of 92 residents and 4 of 79 staff infected.There was no evidence of the development of genotypic resistance, even at low levels, to oseltamivir in patients tested whilst on treatment or prophylaxis. Conclusions: There was no clinical or genotypic evidence of oseltamivir resistance, an important observation in the context of recent reported antiviral resistance in other influenza A subtypes.
Highlights
neuraminidase inhibitors (NI) resistance with influenza A (H1N1) strains
In the 2007/08 winter in the United States, 84 of 1,018 (8.3%) influenza A viruses (all influenza A (H1N1) strains), but none of 135 influenza B viruses, were found to have the H274Y neuraminidase gene mutation associated with high-level oseltamivir resistance (CDC, 2008)
Similar resistance mutations have been detected in influenza A (H1N1) isolates collected in the last quarter of 2008; with very high rates globally (91%) (WHO, 2008)
Summary
NI resistance with influenza A (H1N1) strains. In the 2007/08 winter in the United States, 84 of 1,018 (8.3%) influenza A viruses (all influenza A (H1N1) strains), but none of 135 influenza B viruses, were found to have the H274Y neuraminidase gene mutation associated with high-level oseltamivir resistance (CDC, 2008). Similar resistance mutations have been detected in influenza A (H1N1) isolates collected in the last quarter of 2008; with very high rates globally (91%) (WHO, 2008). This resistance has generally occurred in the absence of oseltamivir treatment, and these viruses have been readily transmitted from person-to-person. Antiviral drug resistance detection has required cell-culture methods to isolate viral strains, followed by genotyping or phenotyping analyses. Potential problems with sequencing include reduced sensitivity for low levels of resistant viral quasispecies, relatively high cost, and difficulty with high throughput and rapid processing. More sensitive methods include the use of padlock probes that allow parallel, high-throughput single nucleotide polymorphism (SNP) genotyping at increased scales. The recent worldwide emergence of increasing oseltamivir resistance to influenza A H1N1 may have important implications for influenza prevention and control
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