Health & Medicine, UK (Commonwealth Union) – A new study has found a vital human gene responsible for halting a majority of avian flu viruses from being transferred into people.
Researchers indicate that knowledge of the genetic make-up of presently circulating avian flu strains can provide better protection against extensive human transmission.
A recent international study conducted by scientists at the MRC-University of Glasgow Centre for Virus Research (CVR) and published in Nature has shed light on the potential of avian flu to cause a pandemic. The study revealed that the human gene BTN3A3, commonly expressed in our airways, plays a crucial role in defending against avian flu. Extensive testing conducted by the research team demonstrated that the BTN3A3 gene serves as a vital defense mechanism, effectively preventing most strains of the virus from breaching human defenses.
Avian flu, also known as bird flu, primarily spreads among wild birds such as ducks and gulls. It can also infect domestic and farmed birds like chickens, turkeys, and quails. Since 2022, there has been a global increase in bird flu cases affecting both wild and domesticated bird populations. Although the disease primarily impacts birds, there have been rare instances of transmission to other species, including humans. Notably, the 1918 Spanish flu pandemic, which caused millions of deaths worldwide, is believed to have originated from an avian strain, according to researchers.
Researchers also indicated that however, despite significant advancements, scientific understanding of avian influenza viruses still has notable gaps. This lack of knowledge makes it challenging to predict which variant of the virus may spill over into the human population and when it might occur.
In their quest to understand the factors contributing to avian flu transmission in humans, the researchers behind this significant study conducted a thorough comparison of gene behavior during viral infections. They examined hundreds of genes typically expressed by human cells when infected with either human seasonal viruses or avian flu viruses. The findings revealed that the BTN3A3 gene played a critical role in inhibiting the replication of avian flu in human cells. However, in contrast, seasonal human flu viruses, which regularly infect the human population, were found to be resistant to BTN3A3, rendering it ineffective against them.
The research team also delved into avian flu viruses that occasionally infect humans, such as H7N9. Since 2013, H7N9 has infected over 1,500 individuals with a 40 percent case fatality rate. Through their investigation, the scientists discovered that avian flu viruses like H7N9 possess a genetic mutation that enables them to evade the inhibitory effects of the BTN3A3 gene, essentially escaping its defenses.
Furthermore, the researchers explored the evolution of avian flu strains and made an observation. They found a simultaneous increase in the prevalence of BTN3A3-resistant strains circulating among poultry at the same time as instances of spill-over events in humans.
Overall, this study provides valuable insights into the mechanisms behind avian flu transmission to humans, shedding light on the role of the BTN3A3 gene and the genetic adaptations of avian flu viruses that enable them to breach human defenses.
Professor Massimo Palmarini, who is Director of CVR, who led this study, with others says “We know that most emerging viruses with human pandemic potential come from animals. It is therefore critical to understand which genetic barriers might block an animal virus from replicating in human cells, thereby preventing infection.”
“Of course, viruses are constantly changing and can potentially overcome some of these barriers by mutating over time. This is why virus genetic surveillance will be crucial to help us better understand and control the spread of viruses with zoonotic and pandemic potential.”
The findings are likely to draw further attention to the significance of BTN3A3 gene for future treatment of zoonotic viruses.
