Effect of age on viral infections: possible role of interferon

In both experimental animals and humans, three stages of susceptibility to viral infections are apparent: 1) the neonatal state, characterized by enhanced susceptibility to infections; 2) childhood and adolescence, during which there is decreased susceptibility; and 3) adulthood (sexual maturity), characterized by increased susceptibility to primary viral infections with advancing age. Moreover, advanced age is associated with reactivation of latent viruses, most notably VZV, and, most likely, oncogenic viruses as well. The mechanisms responsible for these alterations in susceptibility to viral infections have not been completely elucidated. Differences in antibody production do not seem to play a role. Most authors feel that depression of cell-mediated immunity, as measured by delayed cutaneous hypersensitivity or lymphocyte stimulation by mitogens and antigens may be of importance. There have been, however, only few studies on the role of antiviral moieties, such as the interferon(s). Our data on interferon formation in response to coxsackievirus B3 infection in mice suggest that adult mice produce relatively less interferon in relation to the amount of virus replicated in their tissues than do younger animals. Furthermore, the absolute amount of interferon produced by adult animals in response to intravenous injection of (non-replicating virus) NDV was less than that found in younger mice. We report our studies on interferon with no implication that these data supply an adequate explanation for the greater vulnerability of adult mice infected with coxsackievirus B3. It is unlikely that the matter of age and susceptibility has interferon (or indeed any other factor) as a single determinant.(ABSTRACT TRUNCATED AT 250 WORDS)