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Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines
Published on: November 8, 2011
Latent Membrane Protein 1 of Epstein-Barr Virus Promotes RIG-I Degradation Mediated by Proteasome Pathway
Chongfeng Xu1, Lei Sun2, Wenjun Liu2
1Genetic Resources Center, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Abstract:
RIG-I signaling is critical to host innate immune response against RNA virus infection, and also can be activated against many kinds of cancer. Oncogene LMP1 of Epstein-Barr virus (EBV) contributes to various tumors progress. In this study, we have provided strong evidence that LMP1 inhibits Sendai virus mediated type I interferon production and downregulates RIG-I signaling pathway by promotion RIG-I degradation dependent on proteasome. Nineteen kinds of E3 ligase are identified by IP-MS as LMP1-interactors, they are candidate E3s, which are possibly recruited by LMP1 to mediate RIG-I degradation. CHIP is among these E3s, which has been reported to lead RIG-I degradation. Notably, we find C666-1, an EBV-positive nasopharyngeal carcinoma cell line, expresses low level of RIG-I, even treated with IFN-α, RIG-I expression could not be induced. This evidence indicates that EBV employs a unique strategy to evade RIG-I mediated immune responses.
Insights
Epstein-Barr virus (EBV) oncogene LMP1 degrades RIG-I, inhibiting the innate immune response. This viral strategy evades immune detection in cancers like nasopharyngeal carcinoma.
Area of Science:
- Immunology
- Virology
- Oncology
Background:
- RIG-I signaling is crucial for innate immunity against RNA viruses and cancer.
- Epstein-Barr virus (EBV) oncogene LMP1 promotes tumor development.
Purpose of the Study:
- To investigate how EBV's LMP1 affects RIG-I signaling and innate immunity.
- To identify mechanisms by which LMP1 inhibits antiviral responses.
Main Methods:
- Immunoprecipitation-Mass Spectrometry (IP-MS) to identify LMP1-interacting E3 ligases.
- Analysis of RIG-I expression and degradation in EBV-infected cells.
- Interferon-alpha (IFN-α) treatment to assess immune response induction.
Main Results:
- LMP1 promotes proteasome-dependent degradation of RIG-I.
- Nineteen E3 ligases, including CHIP, were identified as potential LMP1 interactors.
- EBV-positive nasopharyngeal carcinoma cells (C666-1) showed low RIG-I levels, resistant to IFN-α induction.
Conclusions:
- EBV utilizes LMP1 to suppress RIG-I signaling, thereby evading host immune surveillance.
- LMP1-mediated RIG-I degradation is a key viral immune evasion strategy.
- Targeting this pathway could offer new therapeutic strategies for EBV-associated cancers.
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