The health risks to humans are increasing due to avian influenza viruses, as they can multiply at temperatures higher than normal fever, which is one of the body's defense mechanisms to stop viruses

The health risks to humans are increasing due to avian influenza viruses, as they can multiply at temperatures higher than normal fever, which is one of the body's defense mechanisms to stop viruses

A new study by the universities of Cambridge and Glasgow has shown how a specific gene helps these viruses withstand high temperatures, which explains their potential danger to humans.

Human influenza viruses cause millions of infections annually. The most common type, influenza A viruses, tend to replicate in the upper respiratory tract at around 33 degrees Celsius, rather than in the lungs of the lower respiratory tract, where the temperature is around 37 degrees Celsius.

 Fever, one of the body's natural defensemechanisms, sometimes raises the body temperature to 41°C to limit viral replication. However, some viruses, such as avian influenza viruses, can survive and multiply at high temperatures, particularly in the lower respiratory tract or intestines of birds, where temperatures can reach 40–42°C.

The international research team used live mouse models to simulate the effect of fever on the influenza virus. They used a lab-modified human influenza virus known as PR8, which poses no risk to humans.

The results showed that fever effectively inhibits the replication of human influenza viruses; even a slight increase in body temperature is enough to transform a potentially deadly infection into a mild illness. Avian influenza viruses, however, have proven resistant to high temperatures, making them far more dangerous.

The study confirmed that the virus's PB1 gene plays a key role in determining its sensitivity to heat. The ability of viruses to exchange genes, as sometimes occurs when a single host is infected with two viruses simultaneously, may increase the severity of emerging diseases.

Dr. Matt Turnbull, from the University of Glasgow, stated: "The exchange of genes by viruses represents an ongoing threat from new influenza viruses. We saw this during the epidemics of 1957 and 1968, when a human virus exchanged the PB1 gene with a gene from a bird strain, resulting in increased disease severity."

He added: "Monitoring avian influenza strains and testing their resistance to fever may help us identify the most dangerous strains and prepare for a possible outbreak."

Professor Sam Wilson of Cambridge University said: “Although humans are not frequently infected with bird flu viruses, we see dozens of cases annually, with high mortality rates, as in the H5N1 virus, where the mortality rate exceeded 40%.”

He pointed to the importance of understanding what makes these viruses so dangerous to humans, especially in the context of preparing for potential pandemics, stressing that the study's findings could influence infection treatment strategies.

The study was published in the journal Science.


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