Impact of D222G Mutation on H1N1 Influenza Virus
Author Information
Author(s): Jessica A. Belser, Akila Jayaraman, Rahul Raman, Claudia Pappas, Hui Zeng, Nancy J. Cox, Jacqueline M. Katz, Ram Sasisekharan, Terrence M. Tumpey
Primary Institution: Centers for Disease Control and Prevention
Hypothesis
Does the D222G mutation in the hemagglutinin protein affect the receptor binding, pathogenesis, and transmissibility of the 2009 pandemic H1N1 influenza virus?
Conclusion
The D222G mutation does not enhance virus transmission but may increase replication in certain cell types.
Supporting Evidence
- The D222G mutation was associated with severe disease in some patients.
- Ferrets infected with the D222G virus showed similar clinical signs to those infected with the wild-type virus.
- The D222G virus replicated to higher titers in human bronchial epithelial cells compared to the wild-type virus.
Takeaway
Scientists studied a change in the H1N1 virus to see if it made the virus spread more easily or make people sicker, but it didn't help the virus spread better.
Methodology
The study used reverse genetics to introduce the D222G mutation and assessed its effects in ferret and mouse models, along with glycan array analysis.
Limitations
The study's findings may not be generalizable to all strains of H1N1 or other influenza viruses.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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