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Epidemiology, clinical manifestations, and treatment of cytomegalovirus infection in immunocompetent adults

Author
Timothy J Friel, MD
Section Editor
Martin S Hirsch, MD
Deputy Editor
Anna R Thorner, MD

INTRODUCTION

The spectrum of human illness caused by cytomegalovirus (CMV) is diverse and mostly dependent on the host. CMV infections in immunocompromised patients cause substantial morbidity and mortality, especially among transplant recipients and those infected with the human immunodeficiency virus (HIV). Infection in the immunocompetent host is generally asymptomatic or may present as a mononucleosis syndrome. However, occasionally, primary CMV infection can lead to severe organ-specific complications with significant morbidity and mortality [1,2]. Infection of pregnant women, even if asymptomatic, is occasionally associated with the syndrome of congenital CMV in newborns. (See "Cytomegalovirus infection in pregnancy".)

The manifestations and treatment of CMV infection in immunocompetent adults will be reviewed here. The diagnosis of CMV infections in immunocompetent and immunocompromised patients is discussed separately. CMV infection in neonates, children, and immunocompromised hosts is also presented separately. (See "Overview of diagnostic tests for cytomegalovirus infection" and "Approach to the diagnosis of cytomegalovirus infection" and "Congenital cytomegalovirus infection: Clinical features and diagnosis" and "Congenital cytomegalovirus infection: Management and outcome" and "Acquired cytomegalovirus infection in children" and "Clinical manifestations, diagnosis, and treatment of cytomegalovirus infection in lung transplant recipients" and "Prevention of cytomegalovirus infection in lung transplant recipients" and "Clinical manifestations, diagnosis, and management of cytomegalovirus disease in kidney transplant recipients" and "Pathogenesis, clinical manifestations, and diagnosis of AIDS-related cytomegalovirus retinitis" and "AIDS-related cytomegalovirus gastrointestinal disease" and "AIDS-related cytomegalovirus neurologic disease".)

INFECTION, LATENCY, AND REACTIVATION

Like other members of the Herpesvirus family, cytomegalovirus (CMV) establishes latent infection after the resolution of acute infection. Productive (lytic) infection leads to the synthesis of immediate-early, early, and late viral proteins [3]. Viral DNA has been detected in monocytes, dendritic cells, megakaryocytes, and myeloid progenitor cells in the bone marrow [4].

Secondary, symptomatic disease may present later in the life of the host, reflecting one of two possibilities: reactivation of latent CMV or reinfection with a novel exogenous strain [5]. One prospective study of 205 postpartum seropositive women found that approximately one-third of the participants had CMV reinfection over a mean of 35 months of follow-up [5]. In this study, reinfection was determined by the appearance of new antibodies with strain-specific binding to unique polymorphic determinants on the envelope glycoprotein of cytomegalovirus. A similar frequency of reinfection was noted in a study of healthy seropositive women over 30 months of follow-up; furthermore, CMV viremia and viruria were common, suggesting that naturally acquired immunity to CMV does not alter shedding patterns [6].

Reactivation of CMV may occur at any time during the life of the human host, although the risk is higher in the setting of systemic immunosuppression, either iatrogenic or secondary to underlying medical conditions, such as the acquired immunodeficiency syndrome (AIDS). As an example, in one study, glucocorticoid use was associated with an increased risk of CMV colitis in otherwise immunocompetent adults [7].

                        

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Literature review current through: Nov 2016. | This topic last updated: Wed Oct 28 00:00:00 GMT+00:00 2015.
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