VIRGINIA BEACH—Genes and the proteins they encode could be the key to understanding why the flu virus kills some patients and spares others, suggest the results of 2 studies in mice presented at the American Physiological Society conference.

The first study found that a strain of mice that is more likely to die of the flu virus (type B) mounts a dramatically enhanced immune response in the lungs compared with a strain of mice that typically develops a milder form of the disease (type C). When the same dose of influenza A virus was given to both strains of mice, approximately 50% of the disease-susceptible type B mice died compared with only approximately 10% of the disease-resistant type C mice.

Analysis of early immune response to determine levels of virus, cytokines, and myeloperoxidase revealed that although the virus levels in lung tissue did not differ significantly between strains, levels of all but one of the proinflammatory cytokines were significantly higher in the type B mice.

The second study looked at immune-related messenger RNA (mRNA) levels after the 2 mouse strains had been exposed to the flu. Again, no differences were found in the amount of virus in the lungs, but a significant difference was revealed in immune-related mRNA levels, which were on average 24 times higher in the type B mice than in the  uninfected control mice. In contrast, mRNA levels in type C mice increased by less than 3-fold after infection.