Reacción a "Avian influenza viruses can resist fever"

Influenza viruses are adapted to very different temperatures depending on their host: human strains replicate best in the upper respiratory tract, which is around 33–37°C, while avian strains thrive in the respiratory and digestive systems of birds, where the temperature reaches 40–42°C. Although this difference was known, it had not been studied in depth at the molecular level. The new published work shows—through the use of chimeric viruses and experiments in cells and in a “simulated fever” model in mice—that temperature alone can slow down seasonal flu, but not viruses that have adapted some of their genes, such as the PB1 segment, which allows them to adapt depending on the context, better at higher temperatures, such as those found in birds or the temperature we have when we have a fever.

This finding of PB1-associated adaptation helps explain why fever is an effective defence against common strains adapted to humans and why certain avian viruses can circumvent that barrier and resist, which is interesting as an additional mechanism that could explain the adaptation to species jumping and the increased virulence of avian viruses that have been sources of pandemics, such as the influenza viruses of 1918, 1957 and 1968.

As aspects that remain to be clarified in the future (limitations), the “simulated fever” model used in in vivo experiments in mice does not reproduce the actual temperatures of the human respiratory tract or the respiratory and digestive systems of birds, which are lower; even so, the phenotype remains, suggesting that it does not depend solely on absolute temperature, but on cellular mechanisms adapted to specific temperature ranges that modulate viral activity. Among these, the role of ANP32 proteins stands out, whose variation between species conditions the thermal sensitivity of the viral polymerase and explains why adaptation is not uniform in different animals.

Fever can act as an antiviral defence against seasonal strains that are sensitive to temperature. The indiscriminate use of antipyretics could promote replication. This effect does not apply to avian or pandemic viruses with thermoresistant PB1. Caution is recommended in the management of fever, monitoring of thermal sensitivity as a risk marker, and explaining to patients that moderate fever is part of the defence mechanism.

The current risk of avian influenza to the general population remains low, although there is a global H5N1 panzootic spreading to mammals that requires surveillance. There is no sustained human-to-human transmission. The study explains how some avian viruses could resist the thermal barrier of fever thanks to thermoresistant PB1, which is relevant for preparedness, not alarmism.