Related Experiment Video
Updated: Oct 2, 2026

An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection
Published on: March 30, 2018
Epstein-barr virus can infect B-chronic lymphocytic leukemia cells but it does not orchestrate the cell cycle
A Maeda1, K Bandobashi, N Nagy
1Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden. akimae@eos.ocn.ne.jp
Objectives:
To understand the mechanism for the refractoriness of B-chronic lymphocytic leukemia (B-CLL) cells for Epstein-Barr virus (EBV)-induced immortalization.
Study Design/Methods:
Cultures were initiated with EBV-infected tonsillar B and B-CLL cells. Expression of EBNA-2 and some of the key players regulating G1/S phase transition such as c-myc expression, phosphorylation of Rb protein, expression of G1 cyclins, and the cyclin-dependent kinase inhibitor p27 were followed.
Results:
In line with earlier studies, EBV infection induced c-myc expression, pRb phosphorylation, D2 and D3 expression, and disappearance of p27 in normal B cells. In contrast, EBV-infected B-CLL cells remained resting and they did not express c-myc; cyclin D2, ppRb and cyclin D3 were seen only in occasional cells. Importantly, p27 expression was maintained.
Conclusions:
In B-CLL cells, the expression of the EBV-encoded nuclear proteins EBNAs is not followed by entrance to the cell cycle. Thus, the difference in the interaction of EBV-normal B cells and EBV-B-CLL cells is already apparent early after infection.
Related Concept Videos
Negative Regulator Molecules
Inhibition of Cdk Activity
Abnormal Proliferation
The Intrinsic Apoptotic Pathway
DNA Damage can Stall the Cell Cycle
DNA Damage Can Stall the Cell Cycle

