Braunschweig Helmholtz researchers have found that an excessive immune response is responsible for the fatal outcome of influenza illnesses in mice.
The researchers have also found that this overreaction has genetic roots.
"Where there are many scientific works dealing solely with the flu virus, we have investigated how the host reacts to an infection," says Klaus Schughart, head of the Experimental Mouse Genetics research group.
During the study, the study group injected seven different inbred mouse strains with the same quantity of type Influenza A flu viruses.
While all of the animals within one mouse strain were genetically identical just like identical twins, one strain differed from another just like different individuals in the human population.
The researchers said that their experiments enabled them to identify strong differences in the progression of the influenza between the seven strains.
They revealed that the illness was mild in five of the strains: the animals lost weight, recovering completely after seven to eight days.
However, in two of the mouse strains, the animals lost weight rapidly and died after just a few days.
With a view to finding out the reasons behind those differences, the researchers studied how the immune system of the animals responds to the virus.
"The mice die from their own immune defences, which are actually supposed to protect them against the virus. The immune system produces too many messengers, which have a strong activating effect on the immune cells. These cells then kill tissue cells in the lungs that are infected with the virus," says Schughart.
Simultaneously, the overactive cells also destroy healthy lung tissue, adds the researcher.
In mice that died, the team also found one hundred times more viruses than in animals that survived.
"It appears that the animals have specific receptors on their cells that make them more receptive to a severe viral infection," says Schughart.
The researchers believe that flu infections in humans may also take a similar course, and that factors may favour a severe progression of the illness.
"It is only now that we are beginning to understand the role played by the genetic factors of the host and what increased receptiveness means in the case of influenza," says Schughart.
The study has been published in the scientific magazine PLoS One.