Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

8.0K
The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
8.0K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Systematic investigation reveals extensive Epstein-Barr virus transcriptional regulation of the human genome.

Cell genomics·2026
Same author

Epigenetic Regulation of the Epstein-Barr Virus Latent-Lytic Switch.

Journal of medical virology·2026
Same author

Arginine metabolism supports <i>de novo</i> pyrimidine biosynthesis to block DNA damage and maintain Epstein-Barr virus latency.

mBio·2026
Same author

EBNA1 inhibitors reveal CDC7 and POU2F1 as direct functional targets in EBV epithelial cancers.

mBio·2026
Same author

Anellovirus-Mediated Interferon Dysregulation Enhances Virus-Induced Lung Injury.

American journal of respiratory cell and molecular biology·2026
Same author

CRISPR Screens Reveal Epstein-Barr Virus-activated JunB as a Key Lymphoblastoid B cell Dependency Factor that Represses Cyclin Dependent Kinase Inhibitor P18INK4c.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: Sep 30, 2025

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
09:14

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line

Published on: September 28, 2022

4.1K

Epstein-Barr virus latency programs dynamically sensitize B cells to ferroptosis.

Eric M Burton1,2,3, Jewel Voyer1, Benjamin E Gewurz1,2,3,4

  • 1Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.

Proceedings of the National Academy of Sciences of the United States of America
|March 11, 2022
PubMed
Summary

Epstein-Barr virus (EBV) transformation generates lipid byproducts. Targeting this process with ferroptosis induction offers a potential therapy for EBV-associated lymphomas like Burkitt lymphoma.

Keywords:
B lymphocyteferroptosislipid metabolismoxidative stresstumor virus

More Related Videos

Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines
06:38

Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines

Published on: November 8, 2011

40.6K
Ferritinophagy: Assessing the Selective Degradation of Iron by Autophagy in Human Fibroblasts
09:21

Ferritinophagy: Assessing the Selective Degradation of Iron by Autophagy in Human Fibroblasts

Published on: February 23, 2024

1.1K

Related Experiment Videos

Last Updated: Sep 30, 2025

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
09:14

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line

Published on: September 28, 2022

4.1K
Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines
06:38

Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines

Published on: November 8, 2011

40.6K
Ferritinophagy: Assessing the Selective Degradation of Iron by Autophagy in Human Fibroblasts
09:21

Ferritinophagy: Assessing the Selective Degradation of Iron by Autophagy in Human Fibroblasts

Published on: February 23, 2024

1.1K

Area of Science:

  • Oncology
  • Virology
  • Cell Biology

Background:

  • Epstein-Barr virus (EBV) is implicated in significant human diseases, including Burkitt lymphoma and post-transplant lymphoproliferative disease (PTLD).
  • EBV-driven B cell immortalization into lymphoblastoid cell lines (LCLs) serves as a model for PTLD, involving metabolic reprogramming.
  • Lipid metabolism alterations are crucial for B cell transformation and the development of EBV-associated malignancies.

Purpose of the Study:

  • To investigate the role of lipid metabolism and reactive oxygen species (ROS) during EBV-induced B cell transformation.
  • To determine the necessity of lipid ROS detoxification pathways in early EBV transformation and Burkitt-like B cell outgrowth.
  • To explore the potential of targeting ferroptosis as a therapeutic strategy for EBV-positive lymphomas.

Main Methods:

  • Analysis of lipid ROS generation during different stages of EBV transformation.
  • Assessment of the requirement for glutathione peroxidase 4 and glutathione in lipid ROS detoxification.
  • Induction of ferroptosis by perturbing redox defense mechanisms in transformed B cells and Burkitt cells.
  • Comparison of redox defense dependency between LCLs and early-stage transformed cells.

Main Results:

  • EBV transformation stages produce varying levels of lipid ROS byproducts.
  • A critical phase of Burkitt-like B cell proliferation depends on detoxifying lipid ROS via glutathione peroxidase 4 and glutathione.
  • Disrupting this redox defense in early transformation or Burkitt cells triggers ferroptosis.
  • Lymphoblastoid cell lines exhibit reduced dependence on this specific redox defense, linked to EBV latency programs.

Conclusions:

  • Lipid ROS detoxification is essential for preventing ferroptosis during specific stages of EBV-driven B cell transformation and Burkitt lymphoma development.
  • EBV latency programs influence the reliance on these redox defense mechanisms.
  • Targeting ferroptosis presents a promising therapeutic avenue for managing and treating EBV-associated lymphomas.