Animal models of postinfectious obesity: Hypothesis and review

In a recent review of obesity as a medical problem, it was stated that obesity is so common on a worldwide scale as to replace undernutrition and infectious diseases as themost signiŽcant contribution to ill health (Kopelman, 2000). As noted in a recent editorial, the probable cause of most cases of obesity in humans is thought to be a combination of genetic susceptibility and environmental factors (Rosenbaum and Leibel, 1999). A relatively small number of human cases reported to date are monogenic in origin; these cases represent counterparts of the classical monogenic obesities of rodents (Barsh et al, 2000). The possibility that virus infections might play a role in human obesity development has received little attention despite evidence that viruses can induce obesity in experimental animals. Recent progress relating to mechanisms by which virus infection may lead to obesity development is reviewed, with special reference to neurological infection with canine distemper virus (CDV). To date, viruses from four different taxonomic groups as well as certain strains of the scrapie agent (Carp et al, 1998) have been shown to cause obesity in experimental animals. The diverse group of conventional viruses include the avian retrovirus (RAV-7) (Carter et al, 1983b), a human group D adenovirus, as well as a chicken adenovirus (Dhurandhar et al, 2000, 1992, respectively), strains of Borna disease virus (Narayan et al, 1983), and the morbillivirus, canine distemper virus (CDV). We originally described the unexpected development of morbid obesity in outbred Swiss mice