Avian influenza viruses pose a significant threat to humans because they can replicate even at temperatures higher than typical fever levels. Fever is one of the body's key defense mechanisms, slowing the progression of viral infections. However, new research conducted by scientists from Cambridge and Glasgow has shown that avian flu viruses remain active even under conditions that usually suppress other viruses.

Genetic Features and Pandemics

An article published on November 28 in the journal Science reports the discovery of a gene that significantly affects a virus’s sensitivity to heat. During the influenza pandemics of 1957 and 1968, this gene was transferred from avian viruses to human strains, which contributed to their successful spread. Seasonal influenza A viruses infect millions of people each year, typically multiplying in the cooler upper respiratory tract (around 33°C). In the lower respiratory tract, where the temperature is closer to 37°C, their spread is less effective.

Body Defense Mechanisms

If viruses are not controlled, they can spread throughout the body and cause severe illness. Fever is a natural response that can raise body temperature up to 41°C. Until recently, the mechanisms by which fever slows viruses and the reasons for some viruses’ resistance to high temperatures were not well understood. Avian influenza viruses differ from human strains: they tend to replicate in the lower respiratory tract, and in their usual hosts, such as ducks and gulls, they often infect the intestines, where temperatures can reach 40–42°C.

Experimental Data

Previous studies on cell cultures showed that avian influenza viruses are more resistant to fever-like temperatures than human viruses. The new study, using infected mice, helped clarify how fever protects the body and why this defense may be insufficient against avian strains. Researchers artificially increased the ambient temperature to raise the animals’ body temperature, since mice typically do not develop a fever when infected with influenza A viruses.

The results showed that raising body temperature to fever levels effectively prevented the replication of human influenza viruses, but did not stop avian viruses. An increase of just 2°C could turn a potentially deadly infection with a human influenza virus into a mild illness.

The Role of the PB1 Gene and Genetic Exchange

Researchers found that the PB1 gene, essential for copying the viral genome inside infected cells, plays a key role in temperature resistance. Viruses with the avian variant of the PB1 gene tolerated high, fever-associated temperatures and caused severe disease in mice. This is important because avian and human influenza viruses can exchange genetic material when they simultaneously infect a single host, such as a pig.

The ability of viruses to exchange genes remains a constant threat for the emergence of new influenza strains. This has already happened during past pandemics, when the human virus swapped the PB1 genome with an avian strain, possibly explaining the severe disease in those years. Therefore, it is crucial to closely monitor avian flu strains to be prepared for possible outbreaks. Testing potential viruses for fever resistance can help identify more virulent strains.

Implications for Surveillance and Treatment

Although human cases of avian influenza are rare, dozens of such episodes are recorded annually. The mortality rate from avian flu in humans remains high—for example, in historical H5N1 infections, the fatality rate exceeded 40%. Understanding the reasons for the severe course of avian flu in humans is important for epidemiological surveillance and pandemic preparedness, especially given the threat posed by H5N1 viruses.

According to the researchers, the data obtained may influence future treatment recommendations, although further studies are needed. Fever is often treated with antipyretic drugs such as ibuprofen and aspirin. However, some clinical data suggest that lowering body temperature does not always help patients and may even promote the spread of influenza A viruses in humans.