Epstein-Barr Virus

The Epstein-Barr Virus can be dated back as far as 1958 when it was first associated with the description of Burkett's lymphoma in the malaria belt of east Africa. In 1964, Epstein and Barr isolated continuous cell lines from the Burkett lymphoma cells and an initial description of a herpesvirus was present in these cells. In 1968 the Epstein-Barr Virus was determined to be the etiological agent of infectious mononucleosis and in 1969 it was shown to immortalize lymphocytes in cultures.
Epstien-Barr virus is the causing agent of infectious mononucleosis. This is a disease most common to children and 90 percent of adults show evidence of previous exposure to the virus. The Epstein-Barr virus can be isolated from the saliva of 10-20% of healthy adults and when the saliva is concentrated isolation can occur 100% of the time. Clinically, primary infection with the Epstein-Barr Virus ranges from a mild, self-limited illness in children to infectious mononucleosis in adolescents and adults.
The Epstien-Barr virus has also been linked to several malignant conditions in humans including Burkitt's lymphoma, nasopharyngeal carcinoma, post-transplantation lymphoproliferative disease, non-Hodgkin's lymphomas in patients with AIDS, Hodgink's disease, and now most recently discovered smooth-muscle tumors in immunosuppressed children.
The Epstein-Barr virus is a member of the herpes family. It has a narrow tissue limited to B cells. It can immortalize B cells both in vitro and vivo. The Epstein-Barr Virus genome is a linear DNA, which was the first genome to be completely sequenced. Recent evidence has suggested the Epstein-Barr might be divided into two groups. Group A and group B. They are based on the differences in the protein levels.
Epstein-Barr DNA persists as multiple episomal copies in Lymphocytes and it replicates in sync with the cell chromatin. Tests have proven that the DNA can integrate into cell DNA but it is very rare and is not site specific. In the capsid of the Epstein-Barr genome, the proteins that mediate end ligation are not known. The Epstein-Barr lytic cycle is not induced, but the lytic cycle can be induced by several methods. There are no cell systems for Epstein-Barr growth. The Epstein-Barr genome is a large, double-stranded DNA molecule that encodes more than 100 genes, but out of those 100 genes, only nine are expressed as proteins that have been latently infected and transformed by Epstein-Barr in vitro. These nine genes are responsible for encoding six nuclear antigens and three latent membrane proteins. One of the nuclear proteins and one of the membrane proteins specifically induce the expression of several antigens.
In the Epstein-Barr Virus infection, the body's immune system produces more of substances called heterohil antibodies. These antibodies indicate that an Epstein-Barr infection has entered the body. They are not directed against the virus itself and they do not serve as a protective function. In humans, the Epstein-Barr Virus is thought to initiate infection in the throat. The throat is a very good place for viral replication to occur.
There are two cellular targets infected by Epstein-Barr. The Burkitt's Lymphocytes and epithelial cells. The Epstein-Barr Virus is highly non-lytic therefore there is no plaque assay available for the virus to stay alive. Infection by Epstein-Barr causes the B cells activation. Epstein-Barr enters the latent state in B cells and the entire viral genome is stopped.
In 1964, Epstein and Barr isloted continuous cell lines from Burkitt's lymphoma cells. SOme of the symptoms of mononucleosis are
Bibliography
Liebowitz, David, M.D., Ph. D., "Epstein-Barr Virus-An Old Dog With New

Tricks" The New England Journal of Medicine, January 5, 1995:55-57.

Silverstein, Alvin and Silverstein, Robert and Silverstein, Virginia. Mononucleosis (Diseases and People). Enslow Publishing Company, 1994.
National Institute of Allergy and Infectious Diseases, National Institute of Health, U.S. Department of Health and Human Services, http://fiona.umsmed.edu/~yar/ebv.html, September 1997.