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Related Experiment Videos

[Infection of mutated mouse complement receptor type II by Epstein-Barr virus].

C P Ren1, K Lan, W D Liu

  • 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
PubMed
Summary
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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.

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  • 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.