Pathogenesis

Like other members of the herpesvirus family, the EBV DNA viral genome is encased in a nucleocapsid surrounded by the viral envelope. EBV initially infects oropharyngeal epithelial cells; there, the virus replicates and then primarily infects B lymphocytes (B + EBV) and is disassembled. The genome is thus transported to the nucleus in a state of viral latency. Nearly all seropositive persons actively shed virus in the saliva. During primary viral infection, the EBV-infected B cells rapidly proliferate. The infection is usually brought under control by cytotoxic T cells, and this process often results in infectious mononucleosis. After the acute infection resolves, the virus persists in the peripheral B cells without causing disease; however, in males with X-linked lymphoproliferative disorder, the initial B + EBV proliferation is not contained and may result in fatal mononucleosis (1).

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