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INTRODUCTION

Epstein-Barr virus (EBV) is recognized as the major cause of infectious mononucleosis (IM). Most EBV infections are thought to be spread through saliva. Manifestations of EBV infection are varied and range from asymptomatic infection to fulminant lymphoproliferative disease. EBV is also associated with a number of malignancies, including endemic Burkitt lymphoma, nasopharyngeal carcinoma, Hodgkin disease, and a spectrum of posttransplant lymphoproliferative disease.

PATHOGENESIS AND EPIDEMIOLOGY

EBV is a member of the family Herpesviridae (gamma herpesvirus), which contains linear double-stranded DNA surrounded by a protein capsid with 162 capsomers in an icosahedral arrangement. The nucleocapsid is covered by a lipid-containing envelope derived from the nuclear membrane of the host cell. EBV causes lytic infection of human oropharyngeal and salivary cells and latent infection of human and primate B lymphocytes as well as epithelium of the nasopharynx. It has long been recognized to be lymphotropic for B lymphocytes and to infect both oropharyngeal epithelial cells and myocytes, but it is also true that it infects T lymphocytes and natural killer (NK) cells.

Infection of lymphocytes with linear EBV DNA can transform them into continuously growing lymphoblastoid cell lines containing a circular DNA episome. Once infected, transformed lymphoblastoid cells rarely continue to produce infectious virus in vitro, although EBV antigens can be detected in the cells. The appearance of new antigens on the cell surface of EBV-infected cells is believed to be responsible for the cellular immune response to the virus and for pathogenesis of the resulting disease. The EBV receptor on epithelial cells and B lymphocytes is the CD21 molecule (formerly CR2), which is also the receptor for the C3d fragment of the third component of complement. The virus elicits both humoral and cellular immune responses.

EBV acquired by ingestion appears to first infect either oropharyngeal resting B cells or epithelial cells and then B cells. Subsequently, the virus infects other susceptible B lymphocytes within the lymphoid tissue of the pharynx. During a 30- to 50-day incubation period, virus actively replicates and disseminates throughout the entire lymphoreticular system.

Cell-mediated immune function is essential in the control of and recovery from EBV infection. In EBV IM, the initial infection of B lymphocytes is followed by an extensive proliferation of CD8+ suppressor/cytotoxic T lymphocytes. Subpopulations of these T cells are cytotoxic against EBV-infected lymphoid cells or prevent their proliferation or possibly both. Associated with the increase in these cytotoxic and suppressor cytotoxic T cells is a concomitant decrease in the number of T-helper/inducer cells (CD4+ T lymphocytes), resulting in an inversion of the CD4:CD8 ratio. During lytic infection, several latent viral proteins are also expressed that are kept in check by NK cells and cytotoxic T cells. After convalescence, EBV can be present in memory B cells that express latent membrane protein 2 and EBV nuclear antigen. The virus can undergo reactivation, and some other B cells can undergo lytic ...

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