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Oseltamivir activity against avian influenza H9N2 strain with different point mutations in their neuraminidase

Taha Kumosani1, Diana Ahmadieh, Houssam Shaib

  • 1Biochemistry Department, Faculty of Science and Experimental Biochemistry Unit, King Fahad Medical Research Center, King Abdul Aziz University, P.O. Box 80216, Jeddah, Saudi Arabia.

Veterinaria Italiana
|October 13, 2015
PubMed

Insights

Oseltamivir effectively reduced avian influenza-H9N2 viral propagation in chicken embryos. However, one H9N2 mutant (M1) showed resistance due to neuraminidase mutations, highlighting evolving drug resistance in influenza viruses.

Area of Science:

  • Virology
  • Pharmacology
  • Molecular Biology

Background:

  • Avian influenza virus (AIV) poses a significant threat to poultry and public health.
  • Oseltamivir is a key antiviral medication used to manage influenza infections.
  • Understanding drug resistance mechanisms is crucial for effective antiviral therapy.

Purpose of the Study:

  • To optimize oseltamivir delivery for maximum antiviral activity against avian influenza-H9N2 in chicken embryos.
  • To assess the susceptibility of oseltamivir-treated H9N2 mutants to the drug.
  • To investigate the impact of neuraminidase mutations on oseltamivir resistance.

Main Methods:

  • Chicken embryo model used to test oseltamivir efficacy against avian influenza-H9N2 (P0 strain).
  • Optimized oseltamivir concentration (0.27 mg/100 μl) and viral inoculum (1.2 x 10⁻⁵ HA units) determined.
  • Susceptibility of four H9N2 mutants (M1-M4) to oseltamivir evaluated using the optimized protocol.

Main Results:

  • Oseltamivir achieved a 95% reduction in viral propagation (HA titer) against the P0 strain at the optimized conditions.
  • One mutant (M1) exhibited resistance to oseltamivir, showing minimal reduction in HA titer.
  • Mutants M2, M3, and M4 displayed varying sensitivity, with HA titer reductions of 82.9%, 61.5%, and 100.0%, respectively.
  • Mutant M1 resistance was linked to two adjacent point mutations in the neuraminidase (N) amino acid sequence (positions 46 and 47).

Conclusions:

  • The study successfully optimized oseltamivir delivery in chicken embryos for avian influenza-H9N2.
  • Emergence of oseltamivir-resistant H9N2 mutant (M1) identified, associated with specific neuraminidase mutations.
  • Further research is needed to elucidate the precise mechanism by which neuraminidase mutations influence H9N2 susceptibility to oseltamivir.

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