For centuries people have argued about the nature and value of fever. Hippocrates thought fever could “cook” an illness out of a patient. By the 18th century many doctors viewed fever itself as a dangerous disease that must be treated.
Today fever is recognized as part of the immune response to infection, a reaction shared across many animal species. Still, exactly how higher body temperature helps control infections is not fully understood.
Sam Wilson, a microbiologist at the University of Cambridge, says there are two main possibilities. Fever’s heat might directly damage or slow pathogens, as Hippocrates speculated. Or the warmth could boost immune processes, or simply be an unavoidable side effect of fighting infection. Those unanswered questions motivated Wilson and colleagues to investigate.
Their study, published in Science, suggests that in mice elevated temperature alone can be enough to reduce some viral infections. Disentangling the effect of temperature from the immune response is difficult, so the researchers designed an experiment where temperature could be isolated.
They chose bird flu as a model because birds have higher body temperatures than humans. Influenza A strains that circulate in birds are adapted to replicate in warmer environments—roughly the same temperatures reached in a human fever. The team identified a segment of the bird flu genome, called PB1, that helps the virus thrive at higher temperature, and inserted it into a human influenza virus. This produced two nearly identical viruses: a normal human strain and a heat-tolerant version.
Mice proved useful test subjects because they do not mount a fever in response to influenza infection. The researchers simulated a fever by housing some mice at slightly elevated ambient temperatures, then exposed animals to either the normal or the heat-tolerant virus.
At standard lab temperatures, mice infected with either strain became ill. But at the higher housing temperature, a clear difference appeared: mice infected with the normal human-adapted strain were largely spared, while those infected with the heat-tolerant strain still became sick. That result supports the idea that temperature alone can impede certain viruses.
Daniel Barreda, a microbiologist not involved in the research, says the study reinforces temperature as an important antiviral factor, though it doesn’t rule out that fever also enhances immune function—especially for viruses less temperature-sensitive than influenza. Joe Alcock, an emergency physician and researcher, praises the work but cautions against assuming the findings translate directly to humans.
The study contributes to evidence that fever may have evolved for a reason. It also raises practical questions about routine suppression of fever with medications like acetaminophen or ibuprofen. While treating fever can be necessary—high temperatures can damage human cells—the possibility that antipyretics might impede viral clearance remains unresolved.