Multiple roles of LMP1 in Epstein-Barr virus induced immune escape

Semin Cancer Biol. 2008 Dec;18(6):388-96. doi: 10.1016/j.semcancer.2008.10.004. Epub 2008 Nov 1.


The life cycle of Epstein-Barr virus (EBV) is intriguing in that the virus resides within the immune system and utilizes distinct latency expression programs to establish a persistent infection yet escaping elimination. To achieve this EBV has hijacked cellular signaling pathways to its own benefit, but deregulated viral gene expression can turn into oncogenesis. EBV like many other persistent herpes viruses has evolved ingenious tricks to evade the immune system in part by mimicking host gene function(s). Latent membrane protein 1 (LMP1) mimics CD40 signaling as part of its "normal" biological function and when deregulated, functions as a viral oncogene. LMP1 also affects cell-cell contact, cytokine and chemokine production, Ag presentation and is secreted in the extracellular milieu via immunogenic exosomes. Thus, besides its well-known growth promoting properties LMP1 modulates immune responses. Herein we discuss current knowledge regarding the role of LMP1 in immune evasion of EBV and how this strategy for establishment of persistence contributes to immune escape of EBV+ tumors.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amino Acid Sequence
  • B-Lymphocytes / cytology
  • B-Lymphocytes / immunology
  • B-Lymphocytes / metabolism
  • B-Lymphocytes / virology*
  • CD40 Antigens / immunology
  • CD40 Antigens / metabolism*
  • Epstein-Barr Virus Infections / immunology*
  • Epstein-Barr Virus Infections / virology
  • Herpesvirus 4, Human / immunology*
  • Humans
  • Molecular Sequence Data
  • Sequence Alignment
  • Signal Transduction
  • Tumor Escape / immunology*
  • Viral Matrix Proteins / immunology
  • Viral Matrix Proteins / metabolism*


  • CD40 Antigens
  • EBV-associated membrane antigen, Epstein-Barr virus
  • Viral Matrix Proteins