Three mutations switch H7N9 influenza to human-type receptor specificity

Area of Science:

• Virology
• Molecular Biology
• Public Health

Background:

• The 2013 avian H7N9 influenza outbreak involved novel human transmission.
• A common hemagglutinin (HA) mutation (Q226L) in H7N9 isolates suggested adaptation to human receptors.
• This mutation, previously linked to pandemic influenza viruses, did not confer human-type receptor specificity in H7N9.

Purpose of the Study:

• To investigate the potential of H7N9 hemagglutinin (HA) to acquire human-type receptor specificity.
• To identify specific mutations enabling H7N9 adaptation to human respiratory tissues.

Main Methods:

• Mutation analysis of the H7N9 hemagglutinin (HA) protein.
• Assessing viral receptor binding specificity.
• Evaluating binding affinity to human trachea epithelial cells.

Main Results:

• The Q226L mutation alone was insufficient to switch H7N9 receptor specificity from avian to human types.
• Three specific amino acid mutations were identified that conferred a switch to human-type receptor specificity.
• These mutations resulted in binding characteristics similar to the 2009 H1N1 pandemic virus and promoted binding to human trachea cells.

Conclusions:

• The H7N9 hemagglutinin possesses the capacity to adapt to human-type receptors through specific mutations.
• These findings highlight the potential for H7N9 to adapt for efficient human transmission.
• Further surveillance and research are crucial for pandemic preparedness.