Demographics:

• General: Approx. 90–95% of adults are EBV-seropositive worldwide.
• Peak incidence (of symptomatic disease): 15–24 years of age

Aetiology:

• Epstein Barr Virus (Human herpes virus 4 – HHV-4) γ Herpesvirus

Disease course:

• Acute: Inf. Mononucleosis (epithelial, URTI)
• Latent in B Cells later reactivation.
• Virus may kill B. Ly or latent within Nucleus of B lymphocytes. altered B lymphocytes produce Heterophile & auto antibodies → reactivation → Neoplasms: B cell lymphoma & nasopharyngeal Ca.

Pathogenesis

EBV droplets/saliva → URTI → viral transfer from mucosal epithelium to B lymph → lymphatic spread (latent) → latent autoAb production and dissemination → reactivation and neoplasia

• Transmission: Infectious mononucleosis spreads via bodily secretions, especially saliva.
• EBV infects B lymphocytes in mucosal epithelium (oropharynx, cervix) via the CD21
• Infected B lymphocytes induce a humoral (B-cell) as well as a cellular (T-cell) immune response. The T-cell immune response causes an increased concentration of atypical lymphocytes in the bloodstream, which are CD8+ cytotoxic T cells that fight infected B lymphocyte