The highly pathogenic H7N3 avian influenza strain from July 2012 in Mexico acquired an extended cleavage site through recombination with host 28S rRNA

Table 2 Comparison of residues at key sites shown to be important for potential human-to-human transmission

Residue position	Wildtype residue in H5	Adaptation mutant residue in H5	Observed residue, 2012 H7N3
110 (103)	H	Y	Q
160 (156)	T	A	A*
158 (154)	N	D	N
224 (220)	N	K	N
226 (222)	Q	L	Q
228 (224)	G	S	G
318 (315)	T	I	T

In order to examine the likelihood of efficient airborne human-to-human transmission of the 2012 H7N3 viruses, wildtype and mutant residues at previously identified key positions making H5 viruses transmissable in ferrets[33, 35] were compared to the corresponding residues in the hemagglutinin amino acid sequence for H7N3. Listed residue positions are based on H3 numbering as used in Imai et al. followed by alternative numbering as in Herfst et al. in parenthesis. An asterisk * indicates the single position where the new strain has a mammalian transmission-adapted rather than the avian wildtype residue.