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Biased mutational pattern and quasispecies hypothesis in H5N1 virus
Ramona Alikiiteaga Gutiérrez1, Alain Viari, Bernard Godelle
1Virology Unit, Institut Pasteur in Cambodia, Réseau International des Instituts Pasteur, 5 Monivong blvd, PO Box 983, Phnom Penh, Cambodia.
Summary
Highly Pathogenic Avian Influenza (HPAI) H5N1 virus mutations in chickens were analyzed. A host-driven adenosine deamination process significantly influenced viral mutations, yet the virus remained infective, aligning with quasispecies theory.
Area of Science:
- Virology
- Molecular Biology
- Genetics
Background:
- Influenza viruses, particularly Highly Pathogenic Avian Influenza (HPAI) H5N1, exhibit high mutation rates due to their segmented RNA genomes.
- Understanding viral mutation dynamics is crucial for tracking pathogen evolution and developing effective control strategies.
Purpose of the Study:
- To investigate the specific mutational events occurring in HPAI H5N1 virus during chicken infection.
- To analyze mutations in key viral genes, including hemagglutinin (HA), neuraminidase (NA), PB2, and NS proteins.
Main Methods:
- Experimental infection of chickens with a lethal dose of HPAI H5N1 virus.
- Collection of lung, spleen, and brain tissues for viral analysis.
- Polymerase Chain Reaction (PCR) amplification and sequencing of viral gene fragments.
- Analysis of mutations after multiple viral replicative cycles.
Main Results:
- A significant mutational bias was observed, with 81% of mutations resembling host-driven ADAR1 adenosine deamination.
- RNA-dependent RNA polymerase-related mutations were present at frequencies compatible with viral survival.
- Despite high mutation rates, potentially leading to 'error catastrophe,' the HPAI H5N1 virus remained infective.
- The virus exhibited characteristics consistent with quasispecies theory.
Conclusions:
- The study highlights the substantial role of host-driven ADAR1-like activity in shaping HPAI H5N1 viral mutations during infection.
- The findings suggest that HPAI H5N1 virus possesses mechanisms to tolerate high mutation frequencies, consistent with quasispecies dynamics.
- The interplay between host-induced mutations and viral quasispecies structure is critical for HPAI H5N1 infectivity and survival.
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