Human Gene BTN3A3 Implicated in Blocking Bird Flu Viruses from Infecting People
Key Highlights :
The UK has been at the forefront of research into the human response to bird flu viruses, with a team of scientists from the MRC-University of Glasgow Centre for Virus Research studying hundreds of genes normally expressed by human cells. Their findings, published in the science journal Nature, have homed in on a gene called BTN3A3, which appears to be a key factor in whether any bird flu strain has human pandemic potential.
Bird flu, also known as avian influenza, chiefly spreads among wild birds such as ducks and gulls and can also infect farmed birds and domestic poultry such as chickens, turkeys and quails. Although the viruses largely affect birds, they can spill into bird predators, and in rare cases, humans typically in close contact with infected birds. The research team compared the genes' behavior during infection with either human seasonal viruses or avian flu viruses, and found that the BTN3A3 gene blocks the replication of most strains of bird flu in human cells.
Nicknamed B-force by the researchers, the gene is part of a broader defensive apparatus in the human immune arsenal against bird viruses. All the human influenza pandemics, including the 1918-19 global flu pandemic, were caused by influenza viruses that were resistant to BTN3A3. However, the gene's antiviral activity failed to protect against seasonal human flu viruses.
The research is particularly timely given the emergence of a new H5NI strain of bird flu that transmits easily among wild birds. This strain has explosively spread into new corners of the globe, infecting and killing a variety of mammal species and raising fears of a human pandemic. So far, only a handful of human cases have been reported to the World Health Organization (WHO). About 50% of H5N1 strains circulating globally so far in 2023 are resistant to BTN3A3, said professor Massimo Palmarini, the corresponding author of the study.
The research highlights the importance of paying particular attention to bird flu strains that are resistant to BTN3A3, as this could indicate an elevated level of risk. However, viruses mutate all the time, and this does not mean that bird flu viruses could not evolve to escape the activity of BTN3A3.
The findings of the research team have the potential to help inform public health strategies in the event of a bird flu pandemic. By understanding the role of the BTN3A3 gene, scientists can better assess the risk of any given bird flu strain, and take the necessary steps to protect the public from infection.
