Herpesvirus Infections in Organ Transplant Recipients

Abstract

Despite great advances in organ transplantation in the last four decades, herpesvirus infections remain a major cause of morbidity and mortality for a majority of transplant recipients. Central to all herpesvirus infections is the virus’s ability to establish latent, nonproductive infections which can be reactivated at later times in the host’s life, resulting in recurrent infections and associated diseases. While improvements in immunosuppressive drug regimens have decreased the risk of organ rejection, they have not restored the immune competence necessary for the control of primary or reactivated herpesvirus infections. This failure has been offset to a significant degree by the advent of improved techniques for viral diagnosis and monitoring and of new, potent antiviral drugs for prophylaxis and treatment of herpesvirus infections. However, infections caused by the eight human herpesviruses continue to challenge the clinical management of transplant recipients. In this minireview, we focus on recent advances in our understanding of and ability to control herpesvirus infections in organ transplant recipients. CMV. Human cytomegalovirus (CMV; human herpesvirus 5) is a member of the betaherpesvirus subgroup. In developed countries, approximately 40 to 60% of the population has been infected with this virus, and the infection rate increases with age (70). Transmission requires direct contact with infectious virus, which can be shed in the tears, urine, saliva, semen, breast milk, and cervical secretions of infected individuals. The virus can also be transmitted by blood and blood products and by transplantation of infected organs and can be passed vertically from mother to fetus or mother to child (81). In an