Bird flu viruses worry scientists because they keep multiplying at fever temperatures. Fever usually slows viruses, yet new research from Cambridge and Glasgow shows that avian strains resist heat that disables human strains.
A study published on November 28 in Science identifies a gene that strongly influences heat sensitivity. This gene jumped from bird flu strains to human strains during the 1957 and 1968 pandemics and helped those human strains spread.
Seasonal flu infects millions each year and thrives in cooler upper airways at about 33°C. It spreads less effectively in warmer regions of the respiratory tract, where temperatures reach about 37°C.
How fever limits infection and why bird flu resists it
Viruses spread rapidly when unchecked and can cause severe disease. Fever raises core temperature to as high as 41°C to slow viral growth. Scientists long wondered why some viruses fail in heat while others tolerate it.
Avian influenza behaves differently from human strains. It multiplies in the lower respiratory tract and often infects the gut of ducks and seagulls. These environments can reach 40–42°C.
Earlier cell studies suggested that bird flu tolerates fever temperatures better than human flu. The new research uses mouse experiments to clarify how fever protects the body and why this protection fails against avian strains.
Experiments show why fever slows human flu but not avian flu
The research team recreated fever conditions in mice using a laboratory-adapted human influenza strain called PR8, which carries no risk to people.
Mice do not usually develop fever from influenza A, so the scientists raised the temperature of the mice’s environment. This created a controlled fever-like state.
The results showed that fever-level temperatures sharply reduced the ability of human-origin flu to replicate. The same temperature increase failed to stop avian influenza. A rise of only two degrees turned a normally lethal human-origin infection into a mild one.
The PB1 gene helps bird flu withstand fever
The team discovered that the PB1 gene, vital for copying the viral genome, drives temperature resistance. Viruses carrying an avian-like PB1 gene tolerated fever-level heat and caused severe disease in mice. This matters because bird and human viruses swap genetic material when infecting the same host, including pigs.
Dr Matt Turnbull from the University of Glasgow said the ability of viruses to exchange genes remains a major threat. He noted past pandemics where human strains acquired avian PB1 genes, which likely contributed to serious illness.
He said monitoring bird flu strains remains crucial for preparedness. Testing how resistant spillover strains are to fever may help identify more dangerous variants.
High fatality rates keep bird flu a global concern
Professor Sam Wilson from Cambridge said humans rarely contract bird flu, yet health authorities still report dozens of cases each year. Fatality rates have remained high, including historic H5N1 cases with mortality above 40%.
He said understanding what drives severe disease in humans remains essential for surveillance and pandemic planning. This grows more urgent as avian H5N1 continues to pose a pandemic threat.
Implications for fever treatment and future research
The findings may influence future treatment guidance, although more research is needed. Fever is often treated with common medications such as ibuprofen and aspirin. Some clinical evidence suggests that reducing fever may not always benefit patients and could support influenza A spread.
The research received major funding from the Medical Research Council, with additional support from several European and US institutions.
