Study finds gene linked to increased risk of flu & Covid in Oceania’s indigenous populations
Sydney, Oct 30 (IANS) Australian researchers have identified a previously unknown gene that influences the immune defence among indigenous people across Oceania, according to research published on Wednesday.
The research, which was published by The Peter Doherty Institute for Infection and Immunity in Melbourne, was the first of its kind to comprehensively map natural killer cells in Oceania’s indigenous populations, Xinhua news agency reported.
Natural killer cells are a type of white blood cell that play a crucial role in the body’s first line of immune defence by destroying infected and diseased cells, restricting viruses from replicating in the earliest stages of infection.
The new research found that the highly variable natural killer cell receptor KIR3DL1 in Oceania’s indigenous populations binds more tightly to human leukocyte antigens (HLA) molecules than KIR3DL1 forms that are predominant in other parts of the world.
Researchers said that the tighter binding changes the capacity of natural killer cells to sense and respond to infections.
They said the discovery could explain why indigenous people in Oceania, including Australasia, Melanesia, Micronesia, and Polynesia, are disproportionately affected by severe respiratory viral diseases, such as influenza and Covid-19, and could lead to improved prevention strategies.
“Our analyses of over 1,300 individuals revealed that the frequency of this Oceanic variant was as high as 28 per cent among highland Papuans and around 6 per cent in First Nations people from Northern Australia, which could influence susceptibility to infection,” said Katherine Kedzierska, a senior author of the eight-year study from the Doherty Institute and University of Melbourne.
“Our learnings may inform the design of new vaccines or vaccine regimens and immunotherapies, helping to ensure these agents are effective for the broad sweep of human populations,” she said.
–IANS
rvt/
Comments are closed.