Fever is a defense mechanism. When a mammalian immune system detects infection, it raises core body temperature from approximately 37°C to 39–40°C. Most human-adapted viruses — including seasonal influenza strains — replicate poorly above 37°C. Fever doesn't kill the virus directly. It shifts the thermal environment above the virus's operating range, slowing replication enough for the immune system to catch up.
Avian influenza viruses don't have this problem. Bird body temperatures run between 40 and 42°C — already at or above mammalian fever. Avian flu strains carry a polymerase gene, PB1, that enables efficient replication at temperatures that incapacitate human-adapted influenza. When an avian strain infects a human, the host mounts a fever. The temperature rises to 40°C. The virus continues replicating as if nothing has changed, because 40°C is the environment it evolved in.
The defense was calibrated against a specific enemy. Human influenza viruses, adapted to 37°C hosts, are vulnerable to a 2–3°C thermal overshoot. The defense is the overshoot. Avian influenza, adapted to 41°C hosts, experiences the mammalian fever as a temperature well within its baseline operating range. The same mechanism — raise the temperature — has opposite effects depending on the pathogen's thermal origin.
This isn't resistance in the usual sense. The virus didn't evolve to withstand fever. It arrived from an environment where the temperature the fever produces is normal. The defense failed before the encounter began — not because the virus overcame it, but because it was never relevant. The fever was designed for the caliber of threat the host was used to, and the new threat came from a hotter world.