The Virus

Introduction* Epidemiology* Infection/Diagnosis* Virology* Immunology* Vaccine Development


(4) Structure

The Epstein-Barr virus is a doubled stranded DNA virus with an icosohedral-shaped capsid, and a unique place in the herpesvirus family.  The virus infects squamous epithelial cells as well as B lympocytes via the complement receptor, CR2  (CD21).  EBV contains receptors identical to C3d receptors. (1)


 
Proteins

The major antigens include viral capsid antigen (VCA), EBV-induced membrane antigen, (MA), six EBV-associated nuclear antigens (EBNA, 1,2,3a,3b,3c,-leader protein (LP)), early antigen (EA), which comes in diffuse (D) and restricted (R) forms.  EBNA-1 is found in oncogenic states and is probably responsible for maintaining the viral genome in the episomal state.  It is not recognized by host CD8 T cells and it is the only major antigen found in Burkitt's lymphoma and nasopharyngeal cells.  Transformation of B cells involves EBNA-2 and EBNA-3c.(1)  In cell lines lacking the Bam HI-Y-H gene region for EBNA-2, immortalization of B lympocytes does not occur. (2)  There are two types of the virus, A and B. (1)  See the Immunology section for a more detailed description of viral antigens and their related immune effects.

(5)

 
 
(3) Host Cell Invasion

The major surface glycoprotein, gp350/220 recognizes and binds to CR2 on resting B-cells, the same binding site as C3d.  Activation of CD21(CR2) signals a transduction pathway involving CD19, TAPA-1, and Leu-13.  The surface glycoprotein cross-links this complex, promoting the cell from G0 to G1 with the help of EBNA-2 and EBNA-LP.  This process allows EBV to enter the cells and circularize the linear viral genome.  Circularization is a hallmark of latent infection because it ensures that the viral DNA will be replicated along with the cellular DNA (3).

The virus then undergoes lytic replication in the B-cell and is replicated as the the B-cell population expands.   The cycling blast cell will enter peripheral circulation until the EBV-containing cells are cleared from acute infection, with latent virus remaining in memory B-cells. (see diagram)


 

Back to EBV home page








1. Niederman, J.C., Evans, A.S.  "Epstein-Barr Virus."  Viral Infections of Humans: Epidemiology and Control.  New York: Plenum, 1997.
2. Evans, A.S., Mueller, N.E.  "Epstein-Barr Virus and Malignant Lymphomas." Viral Infections of Humans: Epidemiology and Control.  New York: Plenum, 1997, 895-933.
3. Thorley-Lawson, D.A. "EBV Persistence in Vivo: Invading and Avoiding the Immune Response,"Herpesviruses and Immunity Medveczky, P.G., Friedman, H., Bendinelli, M. eds. New York: Plenum, 1998; 165-190.
4. Transmission Electron Micrograph of Herpesvirus.  Courtesy of Dr. Paul MacMillan and Core Laboratories. Brown University.
5. Ackerman, H.W., Berthiaume, L., Tremblay, M. Virus Life Diagrams.  New York: CRC Press, 1998; 53.