British researchers have identified a human gene that can potentially block most strains of avian influenza from infecting humans.
According to Reuters, avian influenza primarily spreads among wild birds and domestic poultry such as ducks, gulls, chickens, and quails. Although the virus mainly affects animals, humans can occasionally come into close contact with infected birds.
Avian influenza primarily spreads among wild birds and domestic poultry such as ducks, gulls, chickens, and quails. (Photo: Reuters)
A team of scientists from the MRC Virus Research Center at the University of Glasgow studied hundreds of gene samples that are commonly found in human cells, comparing the behavior of these genes during infections with seasonal influenza viruses in humans or avian influenza viruses.
They focused on a specific gene called BTN3A3, present in both the upper and lower respiratory tracts of humans. This gene was found to have the ability to inhibit the replication of most avian influenza strains in human cells. BTN3A3 appears to be a key factor determining whether any strain of avian influenza virus could potentially cause a pandemic in humans.
However, the antiviral activity of this gene does not provide protection against seasonal influenza viruses. Researchers noted that all human influenza pandemics, including the global pandemic of 1918-1919, were caused by influenza viruses resistant to BTN3A3.
Naturally, viruses are always evolving, which means that avian influenza viruses could potentially evolve to escape the effects of BTN3A3.
Earlier this year, a new strain of H5N1 avian influenza that spreads easily among wild birds has expanded globally, infecting and killing many mammal species, raising concerns about a potential pandemic in humans. To date, only a few cases of avian influenza transmission to humans have been reported by the World Health Organization (WHO).
Professor Massimo Palmarini, one of the study’s authors, stated that approximately 50% of H5N1 strains circulating globally as of 2023 are resistant to BTN3A3. “This is something we should pay special attention to as the risk level increases,” warned Sam Wilson, another co-author of the study.
