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Updated: Jul 9, 2026
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Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines
Published on: November 8, 2011
[Infection of mutated mouse complement receptor type II by Epstein-Barr virus]
1Cancer Research Institute, Xiangya Medical College, Central South University, Changsha 410078, China.
Hunan Yi Ke Da Xue Xue Bao = Hunan Yike Daxue Xuebao = Bulletin of Hunan Medical University
|January 23, 2003
Summary
Researchers modified the mouse complement receptor Type II gene (MCR2) to study Epstein-Barr virus (EBV) entry. Human CR2 (hCR2) and mutant MCR2 (mtMCR2) on SP2/0 cells showed EBV infection, with hCR2 cells being more susceptible.
Area of Science:
- Molecular Biology
- Virology
- Immunology
Context:
- Epstein-Barr virus (EBV) entry mechanisms are not fully understood.
- Complement receptor Type II (CR2) is implicated in EBV binding.
- Developing animal models for EBV-related diseases like nasopharyngeal carcinoma (NPC) is crucial.
Purpose:
- To investigate the role of mouse complement receptor Type II (MCR2) in EBV infection.
- To establish cell lines expressing wild-type MCR2, mutant MCR2 (mtMCR2), and human CR2 (hCR2) for EBV interaction studies.
- To compare the susceptibility of these engineered cells to EBV infection.
Summary:
- Site-directed mutagenesis introduced mutations into the MCR2 gene, confirmed by DNA sequencing.
- Eukaryotic expression vectors for wtMCR2/1, mtMCR2/1, and hCR2 were electroporated into mouse SP2/0 cells.
- Stable transfectants were selected using G418 and confirmed via PCR, RT-PCR, and immunohistochemistry.
- Infection with EBV showed that SP2/0 cells expressing hCR2 and mtMCR2 were susceptible, with hCR2 exhibiting a significantly higher infection rate than mtMCR2.
Impact:
- Provides a foundation for understanding EBV cellular entry pathways.
- Facilitates the development of animal models for studying EBV pathogenesis and NPC.
- Highlights the differential role of CR2 variants in EBV tropism.
