Mechanisms of replication of alpha- and betaherpesviruses and their pathogenesis

The diseases caused by herpes simplex virus (HSV) and human cytomegalovirus (CMV) differ and distinct differences in biological properties of these viruses can be noticed at laboratory work. Despite of this, the structure of DNA and the replication cycle of both viruses shows remarkably common features. Analogous proteins encoded by both viruses, act at initiation of viral DNA transcription, at viral DNA synthesis, at nucleocapsid formation and envelopment. On other hand, considerable differences occur during maturation of virions and at their egress from infected cells. Both viruses in question developed strategies to escape immune recognition by cytotoxic T cells and/or to interfere with the antibody response. Both viruses are widespread in human population and are able to establish latency. Finally, their prevention and/or prophylaxis by effective vaccines has not been solved. Recently, the significance of both viruses has increased. HSV2 is an important pathogen acquired by sexual contact, while CMV reactivates under immunosuppression (post-transplantation, tumours, combined activation in the presence of human immune deficiency virus) and/or causes congenital infection. Chemotherapy of HSV mediated diseases seems more effective than that of CMV mediated infection, because the CMV inhibitor ganciclovir is much more toxic than the CMV inhibitor acyclovir and its derivatives. (Tab. 6, Fig. 5, Ref. 52.)