A RECENT study has uncovered that a single mutation in the H5N1 influenza virus, which recently infected dairy cows in the USA, could significantly enhance its ability to bind to human cells. The research stresses the urgent need for close monitoring of H5N1’s evolution, as this adaptation could increase the risk of human-to-human transmission.
Avian influenza viruses typically require several mutations to spread among humans, but this research reveals that a single amino acid change in the hemagglutinin protein of the H5N1 strain, mutation Q226L, can enable the virus to target human-type glycan receptors, making it the first-reported human-infecting bovine H5N1 virus (A/Texas/37/2024).
The study tested the mutation’s impact using advanced binding assays, which simulate how viruses interact with host cells, and demonstrated that the Q226L mutation greatly enhanced the virus’s attachment to human-like receptors. While additional mutations would likely be needed for efficient human-to-human transmission, the authors also noted that mutations in other viral proteins, such as the PB2 protein, could further aid adaptation to humans. Moreover, the potential for reassortment between H5N1 and seasonal flu viruses during co-infection could accelerate the emergence of a new pandemic strain.
Historically, multiple mutations, typically three or more, have been required for avian influenza viruses to adapt to humans. For the H5N1 2.3.4.4b strain, the potential for easier adaptation raises concerns, particularly as the virus continues to infect a range of species, including humans exposed to contaminated environments or infected animals. While there is no evidence of efficient human-to-human transmission of H5N1 at present, the study highlights the critical need for proactive surveillance.
Ada Enesco, EMJ
Reference
Lin TH et al. A single mutation in bovine influenza H5N1 hemagglutinin switches specificity to human receptors. Science. 2024;386(6726):1128-1134.
