Pathogenicity: animal models.

Abstract

Animal models offer the opportunity to study the interaction of the virus and the host and to unravel the mechanism in processes such as persistence of the virus and virus-induced pathology. Primary infection results in a generalized infection as shown by the presence of virus in many organs. During viraemia the virus is present in mononuclear cells by which it is transported through the body. In neonates and in immuno-suppressed animals the infection results in multiorgan failure, leading to death. Recent data have shown that infection of endothelial cells in the microvasculature and mononuclear cells seems to be important in the pathogenesis of cytomegalovirus (CMV)-induced disease. After primary infection the virus persists in the body. Although the exact localization of the latent virus is unknown it is clear that during latency viral DNA is present in many organs. By immune suppression the virus can reactivate from its latent state. In addition to the direct complications attributable to the virus itself, CMV has modulating effects on the immune response. Although in some instances the infection leads to immune suppression, the virus infection can also accelerate inflammatory and immune responses. Studies in mice have shown that CMV infection 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 response is involved. Although the exact mechanism is not clear, recent data indicate that cytokines, such as tumor necrosis factor alpha are involved in these processes.