Introduction

Nonspecific pharmacological immunosuppression has to be used after transplantation to prevent rejection of the allograft (see Chapter 18); this puts the recipient of a transplant at risk from a number of medical complications including infection. Cytomegalovirus (CMV) is currently the most common opportunistic pathogen to affect this patient group. CMV infection typically becomes apparent one to four months after transplantation [1]. Prior to the development of strategies to control CMV, this infection had a high mortality rate, especially in those lung transplant recipients who developed respiratory failure due to CMV pneumonitis [2, 3]. Currently, CMV still causes considerable morbidity, and occasional mortality, in thoracic organ transplant recipients and adds to the cost of transplantation [4]. In addition, CMV infection appears to predispose to some of the long-term complications of transplantation including transplant-associated coronary vascular disease and bronchiolitis obliterans syndrome [5–7].

Cytomegalovirus

CMV is a human herpes virus of the beta subfamily, systematically designated as human herpes virus 5 (HHV-5) [8]. Like other members of the family, it is a double-stranded DNA virus and has a large genome. Initial CMV infection in an immunocompetent individual is often asymptomatic or only mildly symptomatic. Infection results, however, in a life-long latent infection that can be reactivated or transmitted in circumstances such as organ transplantation.

CMV is a ubiquitous virus and about 60% of the adult population are seropositive indicating prior (and latent) infection. A number of clinical syndromes are associated with CMV, including congenital infection, an infectious mononucleosis-like illness and more severe disease in those immunocompromised after solid organ or bone marrow transplantation or by cancer or human immunodeficiency virus (HIV) infection.