PATHOGENICITY - ANIMAL-MODELS

Animal models offer the opportunity to study the interaction of the vi rus and the host and to unravel the mechanism in processes such as per sistence of the virus and virus-induced pathology. Primary infection r esults in a generalized infection as shown by the presence of virus in many organs. During viraemia the virus is present in mononuclear cell s by which it is transported through the body. In neonates and in immu ne-suppressed animals the infection results in multiorgan failure, lea ding to death. Recent data have shown that infection of endothelial ce lls in the microvasculature and mononuclear cells seems to be importan t in the pathogenesis of cytomegalovirus (CMV)-induced disease. After primary infection the virus persists in the body. Although the exact l ocalization of the latent virus is unknown it is clear that during lat ency viral DNA is present in many organs. By immune suppression the vi rus can reactivate from its latent state. In addition to the direct co mplications attributable to the virus itself, CMV has modulating effec ts on the immune response. Although in some instances the infection le ads to immune suppression, the virus infection can also accelerate inf lammatory and immune responses. Studies in mice have shown that CMV in fection can exacerbate graft-versus-host reactions, and experiments in rats using allogeneic transplants indicate that CMV infection results in enhanced chronic rejection in which acceleration of the immune res ponse is involved. Although the exact mechanism is not clear, recent d ata indicate that cytokines, such as tumor necrosis factor at are invo lved in these processes.