At the height of the seasonal influenza epidemic, research published in the journal Science provides information that may have implications for human health.
The study conducted by the Universities of Cambridge and Glasgow (United Kingdom) witnessed this … Bird flu viruses can reproduce at higher temperatures than a typical fever, which is one of the body’s ways of stopping viruses.
The team identified a gene that plays an important role in determining the thermal sensitivity of the virus. In the deadly epidemics of 1957 and 1968, this gene was transferred to human influenza viruses.and the resulting spread of the virus.
Human influenza viruses, especially type A, infect millions of people each year and replicate best in the upper respiratory tract, at around 33°C. If left uncontrolled, it can spread through the body and cause serious illness, although it is not yet fully understood how fever, which can raise the temperature to 41°C, limits its development. However, avian influenza viruses replicate in the lower respiratory tract, and in their natural hosts such as ducks and seagulls, they infect the intestine, where they withstand higher temperatures of up to 40-42°C.
In previous studies using cell cultures, scientists have shown that avian influenza viruses appear to be more resistant to the temperatures typical of human fevers.
The current study uses live models (mice infected with influenza viruses) to explain how fever protects us and why it may not be enough to protect us from bird flu.
The team studied how fever affects influenza viruses in mice. They used a laboratory-modified human virus that is safe for humans. Since mice do not develop fever due to influenza A, they raise the temperature of the surrounding environment to increase their body temperature. They found that the fever effectively stopped the replication of human influenza viruses, but not avian influenza viruses.. An increase in body temperature of just two degrees Celsius was enough to turn the fatal infection into a mild illness.
Fortunately, humans are not infected with bird flu viruses very often.
The research showed that the viral PB1 gene, which is essential for genome replication, largely determines the virus’s sensitivity to temperature. Viruses containing PB1 similar to those found in avian viruses better withstand high temperatures and have caused severe disease in mice. This is important because human influenza and avian influenza viruses can exchange genes when they infect the same host, as happens in pigs.
Epidemics
“The ability of viruses to exchange genes poses a continuing threat to emerging influenza viruses. We’ve already seen this in previous pandemics, such as those in 1957 and 1968, where a human virus swapped its PB1 gene with that of an avian strain. “This may help explain why these epidemics cause serious illness in people,” says Matt Turnbull, first author of the study.
It is critical that we monitor avian influenza strains in preparation for potential outbreaks. Analyzing resistance to viruses that can spread to fever can help us identify more virulent strains.
Now, says Sam Wilson, “Fortunately, humans don’t get infected with bird flu viruses very often, but we still see dozens of human cases a year.
Avian influenza mortality rates among humans Mortality rates have traditionally been alarmingly high, as has been the case with historical H5N1 infections, which caused more than 40% of deaths.
Understanding why avian influenza viruses cause serious illness in humans is critical to pandemic surveillance and preparedness. This is particularly important because of the pandemic threat posed by avian H5N1 viruses.