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, finding that a single amino acid mutation in a key protein would be enough to switch the virus target from avian-type receptors to human-type receptors.
This mutation, labeled Q226L, could act like a new pair of glasses for the virus, allowing it to recognize landing points on human cells. "Our experiments revealed that the Q226L mutation could significantly increase the virus' ability to target and attach to human-type receptors,""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."from animals after being in close contact with them.
The discovery emphasizes the need to track H5N1 closely and continue to monitor for new strains. While an ability to latch onto our receptors is critical for the virus's spread through humans, it doesn't rule out the possibility that other changes may also be required for transmission. "Our study doesn't suggest that such evolution has occurred or that the current H5N1 virus with only this mutation would be transmissible between humans,"Further research is going to be needed to get a full understanding of how a human-to-human strain of this virus might fare in terms of its transmission mechanisms and its stability in human hosts.
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