Microcompetition with latent Epstein-Barr virus causes a transcription factor deficiency, under-expression of retinoblastoma, and classic Hodgkin lymphoma

Hanan Polansky, Adrian Javaherian


Classic Hodgkin Lymphoma (cHL) is characterized by the presence of Hodgkin/Reed-Sternberg (H/RS) cells, the malignant cells of the tumor.1 H/RS cells show two kinds of changes in their retinoblastoma (pRb) tumor suppressor, inactivation through hyper-phosphorylation of the protein, and low concentration caused by under-expression or over-degradation. This commentary concentrates on the under-expression option.


Hodgkin, Lymphoma,tumor

Full Text:



Schwering I, Brauninger A, Klein U, Jungnickel B, Tinguely M, Diehl V et al. Loss of the B-lineage-specific gene expression program in Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma. Blood. 2003;101(4):1505-1512.

Al-Salam S, Awwad A, Alashari M. Epstein-Barr virus infection is inversely correlated with the expression of retinoblastoma protein in Reed-Sternberg cells in classic Hodgkin lymphoma. Int J Clin Exp Pathol. 2014;7(11):7508-7517.

Knight JS, Sharma N, Robertson ES. Epstein-Barr virus latent antigen 3C can mediate the degradation of the retinoblastoma protein through an SCF cellular ubiquitin ligase. PNAS. 2005;102(51):18562-18566.

Polansky H. Microcompetition with Foreign DNA and the Origin of Chronic Disease. New York: The Center for the Biology of Chronic Disease; 2003.

Liu BH, Wang X, Ma YX, Wang S. CMV Enhancer/Human PDGF-Beta Promoter for Neuron-Specific Transgene Expression. Gene Ther. 2004; 11:52-60.

Slobedman B and Mocarski ES. Quantitative Analysis of Latent Human Cytomegalovirus. J Virol. 1999;73:4806-4812.

Adam GI, Miller SJ, Ulleras E, Franklin GC. Cell-Type-Specific Modulation of PDGF-B Regulatory Elements via Viral Enhancer Competition: A Caveat for the Use of Reference Plasmids in Transient Transfection Assays. Gene. 1996;178:25-29.