Experimental models for study of common respiratory viruses.

Numerous epidemiological studies have shown that there is excess respiratory disease morbidity in areas of high atmospheric pollution, implying an interactive effect on the clinical illness associated with these common infections. The principal etiologic agents of human respiratory infections are respiratory syncytial virus (RSV), influenza viruses (IV), parainfluenza virus types 1 and 3 (P1, P3), adenoviruses (AD), rhinoviruses (RV) and Mycoplasma pneumoniae (Mpn). Understanding the pathogenesis of the excess morbidity related to pollutants would facilitate detection of undesirable human health effects and provide a basis for intervention strategies. Through use of experimental model systems the mechanism of toxic effects could be defined (whether microbiological, immunological, pathological or physiological) to provide direction for appropriate studies in the human host. Small animal models of IV and Mpn infections have been available for many years; recently, experimental models of several more common viral diseases have been developed. A parallel to human RSV infections is provided by the ferret: virus replicates in the lungs of infant animals, but only in the noses of adults. The common cotton rat infected with RSV develops small airways lesions which may mimic the pathophysiologic changes of bronchiolitis. Both guinea pigs and Syrian hamsters are susceptible to human P3 virus, developing peribronchiolar and interstitial lesions. Practical small animal models for human AD and RV infections are not available because of the high host-specificity of these agents. Both the RSV and P3 model infections are nonlethal which enables study for long-term sequelae. Recent reports of pulmonary function abnormalities among children suffering bronchiolitis in infancy underscores the importance of defining toxic influences which could play a role by making the initial infections more severe.