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Abstract zur Publikation: Virus load kinetics and resistance development during oseltamivir treatment in infants and children infected with influenza A (H1N1) 2009 and influenza B viruses

Rath B, von Kleist M, Tief F, Karsch K, Tuerk E, Muehlhans S, Louis F, Skopnik H, Schweiger B, Duwe S (2012): Virus load kinetics and resistance development during oseltamivir treatment in infants and children infected with influenza A (H1N1) 2009 and influenza B viruses.
Pediatr. Infect. Dis. J. 31 (9): 899-905. Epub May 10. doi: 10.1097/INF.0b013e31825c7304.

Background: Infants and small children are the most effective transmitters of influenza, while bearing a high risk of hospitalization and adverse disease outcomes. This study aims to investigate virus load kinetics and resistance development during oseltamivir therapy in infants and children infected with influenza A (H1N1) 2009 and influenza B viruses.

Methods: Virus load in nasopharyngeal samples and phenotypic/genotypic neuraminidase inhibitor resistance were determined at baseline, at day 5 and in additional follow-up samples, if available. Patient-specific viral clearance indices CLv(i) were determined along with estimates of the time required to achieve non-detectable virus load.

Results: No evidence of baseline oseltamivir resistance was detected in 36 patients infected with influenza A (H1N1) 2009 (n= 27) or influenza B (Victoria, Yamagata; n= 9) prior to oseltamivir therapy. On average, viral loads were lower for influenza type B (median = 5.9 103/ml) than in drug resistant (median = 2.6 106/ml), and sensitive A(H1N1)2009 (median = 4.8 104/ml), p = 0.04 and p = 0.09 respectively. Times required to achieve non-detectable virus load were significantly longer in drug resistant A(H1N1)2009 (median 15.4 days) compared to drug sensitive A(H1N1)2009 (p = 0.003; median 7.7 days) and drug sensitive influenza B (p = 0.001; median 5 days). No evidence of viral rebound was observed once viral clearance was achieved.

Conclusions: Our data indicate that influenza subtyping in combination with baseline viral load measurements might help to optimize the duration of antiviral therapy in the individual child. Lower than expected virologic response rates in patients without malabsorption or compliance issues may suggest resistance development.

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