New Delhi, Nov 28 (NationPress) Recent findings reveal that bird flu viruses possess the ability to reproduce at temperatures exceeding typical fever levels—one of our body's defensive mechanisms against viruses—thus heightening the risk to humans. Human influenza viruses, responsible for seasonal flu, are classified as influenza A viruses.

Fever acts as a protective barrier against severe infections caused by human flu viruses, with even a modest rise of 2 degrees Celsius in body temperature capable of transforming a deadly infection into a manageable one.

Researchers from the universities of Cambridge and Glasgow, UK, demonstrated that while elevating body temperature to feverish levels effectively inhibits the replication of human flu viruses, it is unlikely to impede avian or bird flu viruses.

In contrast to human flu viruses, avian influenza viruses are known to flourish in the lower respiratory tract. Typically, in their natural hosts, including ducks and seagulls, the virus often infects the gut, where temperatures can reach as high as 40 to 42 degrees Celsius.

"Fortunately, humans are not frequently infected by bird flu viruses; however, we still observe dozens of human cases each year. The fatality rates associated with bird flu in humans have been alarmingly high, particularly in historical H5N1 infections that resulted in over 40 percent mortality," noted Professor Sam Wilson from the Cambridge Institute of Therapeutic Immunology and Infectious Disease.

"Understanding the factors that enable bird flu viruses to induce severe illness in humans is vital for monitoring and preparing for potential pandemics. This is especially critical given the pandemic threat posed by avian H5N1 viruses," Wilson added.

The study, which was published in the journal Science, utilized in vivo models—specifically, mice infected with influenza viruses—to elucidate the protective role of fever and its limitations against avian influenza.

The researchers simulated fever in mice in response to influenza infections by raising the ambient temperature in their environment. This method elevated the body temperature of the mice.

Although mice typically do not exhibit fever in response to influenza A viruses, the team successfully replicated its effects by increasing the temperature in their housing.

The research also uncovered that the PB1 gene of the virus, crucial for the replication of the viral genome within infected cells, plays a significant role in determining temperature sensitivity.

Viruses with an avian-like PB1 gene demonstrated the ability to endure the elevated temperatures associated with fever, leading to severe illness in the mice.