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Epstein–Barr virus 

Epstein–Barr virus

Chapter:
Epstein–Barr virus
Author(s):

M.A. Epstein

and A.B. Rickinson

DOI:
10.1093/med/9780199204854.003.070503_update_002

Update:

Diagnosis—RT-PCR as an adjunct to serological tests.

Treatment—possible role of corticosteroids and antivirals in immunocompetent patients with unusually severe symptoms

Updated on 31 May 2012. The previous version of this content can be found here.
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date: 30 March 2017

Epstein–Barr virus (EBV) is a human herpesvirus with a linear double-stranded DNA genome that is carried asymptomatically by most people. Symptomless primary infection is usual in childhood, establishing a lifelong carrier state where the virus persists as a latent infection of circulating B cells. The virus replicates recurrently in oropharyngeal epithelial cells, with consequent shedding of virus in saliva transmitting infection.

Infectious mononucleosis

If delayed beyond childhood, primary infection causes infectious mononucleosis in up to at least 50% of cases. This is typically characterized by sore throat, fever, anorexia, headache, fatigue, malaise (often disproportionately severe), generalized lymphadenopathy, splenomegaly (60%), hepatomegaly (10%), and jaundice (8%). Diagnosis can be confirmed by the Monospot test (which detects heterophil antibodies that are present in 85%) or the presence of IgM antibodies to virus capsid antigen. Treatment is supportive unless there are complications. Most cases resolve within 1 to 2 weeks; chronic or recurrent forms are described but are very rare. Primary infection in boys with the X-linked lymphoproliferative trait, a rare congenital immunodeficiency, gives severe or fatal disease. In other rare cases, most common in Asia, primary infection of immunocompetent people can lead to ‘chronic active’ EBV syndrome resembling persistent infectious mononucleosis but sometimes fatal.

B-cell tumours

Endemic Burkitt’s lymphoma—all cells of this common malignancy of children in areas of Africa and New Guinea carry the EBV genome. A cofactor, hyperendemic malaria, explains the unusual geographical distribution of the high incidence disease. Presentation is with jaw and other tumours, peripheral lymph nodes and spleen are spared, and progression to death is rapid. Cyclophosphamide treatment is remarkably effective.

Other forms of Burkitt’s lymphoma—a sporadic type occurs at low incidence worldwide. This is EBV-positive in only a few cases; jaw tumours are rare and lymph nodes are involved; response to treatment is poor—combination therapy is required, and survival after relapse is uncommon. Another form, EBV-positive in 30 to 40% of cases, occurs in AIDS patients.

Other lymphomas—where immune cell control over EBV is impaired in immunosuppressed transplant recipients or long-term AIDS patients, expansions of EBV-transformed B cells can occur as acute polyclonal lymphoproliferative lesions or later monoclonal large cell lymphomas. In transplant patients the first treatment is to reduce immunosuppressive therapy. EBV is also linked to Hodgkin’s lymphoma, with the virus genome present in the Reed–Sternberg and mononuclear tumour cells in some 30 to 40% of cases.

Other malignancies and conditions associated with EBV

Undifferentiated nasopharyngeal carcinoma—this epithelial tumour is most common in southern Chinese and Inuit people, and is EBV genome-positive in all cases. Besides virus infection, dietary, genetic, and perhaps herbal remedy cofactors are involved. Radiotherapy is the treatment of choice.

EBV has more tenuous links with salivary gland tumours, some gastric carcinomas, rare smooth muscle tumours of the immunosuppressed, and certain nasal T and NK lymphomas. The nonmalignant lesions of oral hairy leukoplakia in HIV patients are interesting because the squamous epithelial cells forming them are driven by replicating EBV.

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