This mutation gives the virus a foothold on human cells that it didn’t have before, which is why this finding is a red flag for possible adaptation to people, he added.
The study stated that a second mutation, Asn224Lys, gave a better hold to the virus.
“The findings demonstrate how easily this virus could evolve to recognise human-type receptors,” said the first author and a postdoctoral associate at Scripps Research, Ting-Hui Lin.
“A switch in receptor binding preference of human viruses from avian or swine virus progenitors was previously shown for influenza pandemics in 1918, 1957, 1968, and 2009,” the study pointed out.
It also observed that the mutation in question was tested by scientists in a duck and a few humans during the 2010 H5N1 outbreak in Egypt. But it did not demonstrate the virus affecting human receptor binding, unlike now.
Paulson added that their study does not suggest that such an evolution has occurred or that the current H5N1 virus with only this mutation would be transmissible between humans.
He told LiveScience that a high concentration of viral material from cattle, poultry and infected animals is responsible for the infection recorded in humans so far.
The ability to bind to human receptors alone may not be enough to succeed in human-to-human spread, the researchers noted. Other genetic changes — such as mutations in polymerase basic 2 (E627K) — that enable viral replication and bring stability in human cells would probably be necessary for the virus to spread efficiently among humans.
However, researchers who were not part of the study have already highlighted their concerns observed in other cases. A recent study revealed that the mutation PB2-E627K found in Texas showed an increased ability to transmit between ferrets, when exposed via air in an experiment.
Also, the mutation found in a teenager from the Canadian province of British Columbia was similar to Q226L in that both could attach to the glycan receptors found in humans.
The development left scientists feeling concerned.
Scott Hensley, a professor at Penn Institute of Immunology explained on social media platform Bluesky that the hemagglutinin that primarily binds to bird cell receptors was found to infect equivalent receptors in the tissues located in human eyes, the upper respiratory tract and conjunctiva.
The Gln226Leu mutation has previously been flagged in other studies of H5N1, which also indicated the virus’s ability to infect humans.
