New Delhi, Nov 28 Bird flu viruses can replicate at temperatures higher than a typical fever — one of the body’s ways of stopping viruses in their tracks –, increasing the threat to humans, according to new research.
Human flu viruses, which cause seasonal flu, are known as influenza A viruses.
Fever protects against severe infection from human-origin flu viruses, with just a 2 degrees C increase in body temperature enough to turn a lethal infection into a mild disease.
Researchers from the universities of Cambridge and Glasgow, UK, showed that while raising body temperature to fever levels is effective at stopping human-origin flu viruses from replicating, it is unlikely to stop avian or bird flu viruses.
Unlike human flu viruses, avian influenza viruses tend to thrive in the lower respiratory tract. In fact, in their natural hosts, which include ducks and seagulls, the virus often infects the gut, where temperatures can be as high as 40 to 42 degrees C.
“Thankfully, humans don’t tend to get infected by bird flu viruses very frequently, but we still see dozens of human cases a year. Bird flu fatality rates in humans have traditionally been worryingly high, such as in historic H5N1 infections that caused more than 40 per cent mortality,” said Professor Sam Wilson, from the Cambridge Institute of Therapeutic Immunology and Infectious Disease at the University of Cambridge.
“Understanding what makes bird flu viruses cause serious illness in humans is crucial for surveillance and pandemic preparedness efforts. This is especially important because of the pandemic threat posed by avian H5N1 viruses,” Wilson added.
The study, published in the journal Science, used in vivo models — mice infected with influenza viruses — to help explain how fever protects us and why it may not be enough to protect us against avian influenza.
The team simulated in mice what happens during a fever in response to influenza infections. To carry out the research, they used a laboratory-adapted influenza virus of human origin, known as PR8, which does not pose a risk to humans.
Although mice do not typically develop fever in response to influenza A viruses, the researchers were able to mimic its effect on the virus by raising the ambient temperature where the mice were housed (elevating the body temperature of the mice).
The research also revealed that the PB1 gene of the virus — important in the replication of the virus genome inside infected cells — plays a key role in setting the temperature-sensitivity.
Viruses carrying an avian-like PB1 gene were able to withstand the high temperatures associated with fever and caused severe illness in the mice.
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