Two simultaneous mutations in the H5 HA receptor binding site allow it to bind similarly to human viruses, indicating no genetic barrier to reassortment with internal genes of human viruses at the M2 coexpression level.
May inform H5 surveillance priorities; hypothesis-generating for reassortment risks, pending mammalian transmission studies.
The binding specificities of a panel of avian influenza virus subtype H5 hemagglutinin (HA) proteins bearing mutations at key residues in the receptor binding site were investigated. The results demonstrate that two simultaneous mutations in the receptor binding site resulted in H5 HA binding in a pattern similar to that shown by human viruses. Coexpression of the ion channel protein, M2, from most avian and human strains tested protected H5 HA conformation during trafficking, indicating that no genetic barrier to the reassortment of the H5 surface antigen gene with internal genes of human viruses existed at this level.
No takes yet. Share an insight, caveat, or question.
Harvey et al. (2003) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: