EBV is of the and infects B cells. It’s limited host range (B cells) is due to the limited cellular expression of its receptor which is also the receptor for the C3d component of the . This receptor is expressed on and epithelial cells of the oropharynx and nasopharynx. The virus initially establishes a productive infection in the epithelial cells of the oropharynx and is then shed into the saliva (which can also transmit the virus) and accesses B lymphocytes in lymphatic tissue and blood.
During latent infection, cells contain a small number of circular plasmids like EBV genomes that replicate only during cell division. Select immediate early genes are expressed including Epstein-Barr virus nuclear antigen-1 (EBNA-1) which binds OriP and unwinds DNA. Host then synthesize DNA.
EBV is acquired by close contact between persons through saliva. About 70% of the US population is infected with EBV by age 30.
The disease associated with EBV is called Infectious mononucleosis (IM) and is characterized by fever, malaise and lymphadenopathy. It is milder in children then adults.
Individuals lacking T cell immunity are likely to suffer life threatening polyclonal leukemia like B cell proliferative disease upon EBV infection instead of IM. Transplant patients undergoing immunosuppression are at high risk for post transplant lymphoproliferative disorder instead of IM. Similar diseases are observed for AIDS patients. Hairy oral leukoplakia is an unusual presentation of productive EBV infection that causes lesions of the mouth. It is an opportunistic presentation in AIDS patients.
There is no effective treatment for EBV. Latent viral DNA is unaffected by antiviral drugs because it is replicated by the host DNA polymerase complex. There is, however, life-long immunity. Thus there is no chance of getting a second infection as with HSV.