Since its emergence in 1997, the highly pathogenic avian influenza virus (H5N1) has affected wild birds and poultry in more than 10 Asian countries as well as Europe and Africa. A total of 321 confirmed human cases have occurred since late 2003 resulting in 194 deaths and a fatality rate of approximately 60%. Although there are currently some antiviral drugs available for treatment of influenza virus infection, H5N1 has proven resistant to most, therefore emphasizing the need for an effective vaccine.

The influenza A virus M2 protein consists of three structural domains, one of which is a 54-amino acid cytoplasmic tail domain. In a previous study the researchers demonstrated that deleting the M2 cytoplasmic tail caused a growth defect in the H1N1 influenza virus, indicating that the M2 cytoplasmic tail plays a vital role in virus replication. In the current study they created an M2 tail mutant H5N1 virus, vaccinated mice with it and challenged the mice with a lethal dose of influenza virus. Results showed that the mice were protected from death suggesting that the virus could not replicate and could therefore be used as a vaccine.

Here, we demonstrate that an M2 cytoplasmic tail deletion mutant protects mice from lethal challenge with a highly pathogenic H5N1 virus, suggesting the potential of M2 tail mutants as live attenuated vaccines against H5N1 influenza virus infection, say the researchers.

Further Reading

- You can visit the Avian Flu page by clicking here.