ABSTRACT
The clinical syndrome of infectious mononucleosis (IM) is most frequently manifested during adolescence and young adulthood. After the age of 15, primary infection with Epstein-Barr virus (EBV) leads to the clinical syndrome of IM in approximately 30% to 40% cases (1). Filatov and Pfeiffer initially described the IM syndrome at the end of the 19th century (2,3). However, the association between primary EBV infection and IM was first established in 1968 when a laboratory technician in Dr. Werner Henle’s laboratory seroconverted to EBV during the course of classical IM (4). The mononucleosis syndrome includes a clinical triad of pharyngitis, lymphadenopathy, and fever (5). Patients may experience several days of prodromal symptoms including malaise, fatigue, arthralgia, fever, chills, dysphagia, and anorexia (6). As symptoms of sore throat and fever worsen, patients typically seek medical attention. However, the classic symptoms of IM may be mistaken for those of other common infections including streptococcal pharyngitis. IM is a benign lymphoproliferative disorder caused by a disseminating EBV infection in B-lymphocytes and mucosal epithelial cells that may lead to abnormal clinical signs and symptoms involving almost any organ (7). During the acute phase of IM, roughly one in 103 to 104
circulating B-cells are infected with EBV (8,9). They are proliferating, lymphoblastic plasmacytoid cells, are highly immunogenic, and can trigger potent cellular immune activation (10). In fact, EBV replication is predominantly mediated via cellular DNA polymerase in B-cells, resulting in the transformation of B-lymphocytes (11). In contrast, epithelial mucosal cells become lytically infected and release infectious viral particles (12). This results in oropharyngeal EBV shedding as well as presence of infectious EBV particles in genital secretions (13).
