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Scientists have found that avian flu viruses carry a gene that makes them unusually tolerant to heat, rendering one of our key immune defenses—fever—largely ineffective. Instead of slowing the infection, higher temperatures actually help these viruses reproduce.
Researchers at the University of Cambridge and the University of Glasgow have shed new light on why bird flu poses a greater threat to humans than seasonal influenza A. The difference appears to hinge on a single heat-protective gene called BP1.
Why Avian Influenza Thrives Where Human Flu Struggles
Fever is an ancient mammalian defense mechanism that raises body temperature just enough to hinder the growth of many pathogens, including typical influenza A. Seasonal flu viruses adapted to humans grow best in the cooler temperatures of the upper respiratory tract (around 33 °C / 91 °F) and weaken quickly as temperatures near 40 °C (104 °F).
Birds, however, naturally maintain much higher body temperatures—between 40 °C and 42 °C (104–108 °F). Avian influenza viruses, including the dangerous strains that occasionally infect humans, have evolved to replicate efficiently in these hotter conditions.
The researchers set out to determine whether this heat-tolerance trait helps explain why avian influenza causes such severe disease when it infects humans. To test this, they engineered two nearly identical viruses that differed only in their PB1 gene—the “engine” the virus relies on to replicate.
How a Single Gene Alters Virus Behavior Under Fever Conditions
One virus carried PB1 from a human-adapted strain, which breaks down at fever-level temperatures; the other carried PB1 from avian influenza strains, including those present in the 1957 and 1968 pandemic viruses.
This single genetic swap dramatically changed how the viruses behaved, a pattern first seen in cell cultures and later confirmed in mice. At normal temperatures, both versions made the animals seriously ill. Because mice rarely develop fevers in response to flu, the researchers warmed the animals’ environment, raising their core temperature by about 2 °C (3.6 °F).
In this warmer setting, the human-adapted virus struggled—it couldn’t operate properly or replicate, leading to only mild symptoms. The avian-PB1 virus, however, showed no such weakness: it replicated efficiently and caused severe disease, just as it did in mice kept at normal body temperatures.
“This elegant study builds on the simple insight that animals maintain different body temperatures, and demonstrates how that can shape the way viruses behave when they jump between species,” said Professor Wendy Barclay, Chair of the Medical Research Council (MRC) Infections and Immunity Board. “The researchers show that human-adapted influenza viruses replicate poorly when temperatures rise, as happens during fever. In contrast, avian influenza viruses—accustomed to the higher body temperatures of their natural bird hosts—are not restrained by the fever response when they infect mammals.”
PB1 Gene Reassortment
As noted, the most lethal influenza outbreaks of the 20th century involved viral strains whose PB1 gene originated in birds—a fact revealed through extensive genetic sequencing. Influenza A contains eight separate gene segments, and when two strains infect the same cell, they can exchange these segments through reassortment. PB1 is one of the segments most likely to jump between human and avian viruses during this mixing process.
“The capacity of flu viruses to trade genes remains a major driver of risk for emerging strains,” explained Dr. Matt Turnbull, lead author from the Medical Research Council Centre for Virus Research at the University of Glasgow. “We’ve seen this happen in earlier pandemics, like those in 1957 and 1968, when a human influenza virus acquired its PB1 gene from an avian strain. That may help explain why those pandemics produced such severe disease.”
The new research suggests that this small gene might have enabled those pandemic viruses to bypass the human body’s temperature-based defenses, allowing them to cause such widespread and serious illness—and it underscores the potential danger should an avian flu virus successfully jump into humans again.
“It’s essential to keep a close watch on bird flu strains so we can better prepare for possible outbreaks,” said Turnbull. “Assessing how resistant these viruses are to fever could help us pinpoint the strains most likely to cause severe disease.”
Rare but Deadly
Recently, a resident of Washington died from complications after being infected with a novel avian influenza strain not previously seen in humans. While bird flu viruses have not yet become efficient at spreading between people, human infections, though rare, tend to be severe.
“Fortunately, human infections with bird flu remain uncommon, but we still see several dozen cases each year,” said senior author Professor Sam Wilson from the Cambridge Institute of Therapeutic Immunology and Infectious Disease. “Historically, bird flu infections in humans have had alarmingly high fatality rates, such as with H5N1, which caused over 40% mortality.”
“Grasping why bird flu viruses trigger severe illness in humans is vital for effective monitoring and pandemic preparedness,” Wilson added. “This is particularly critical given the pandemic risk posed by avian H5N1 strains.”
Read the original article on: New Atlas
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