AI Article Synopsis
- Epstein-Barr virus (EBV) has a protein called latent membrane protein 1 (LMP1) that helps the virus survive and replicate, while also triggering the host's cell death mechanisms.
- LMP1 influences both anti-apoptotic processes and apoptosis, showing a complex role in viral persistence and host defense, particularly through the activation of CD8+ T cells that initiate cytotoxic responses.
- Targeted therapies that manipulate the Fas-mediated apoptotic pathway could improve cancer treatments for patients with EBV-related conditions, like nasopharyngeal carcinoma, by enhancing their immune response against tumors.
Article Abstract
The genome of Epstein-Barr virus (EBV) encodes proteins essential for malignant transformation, for example, latent membrane protein 1(LMP1). Whereas, LMP1 up-regulates anti-apoptotic proteins to support viral replication, it also potentiates apoptosis, suggesting that a viral protein contributes to the survival of the virus, and it also elicit host defense leading to the destruction of the infected cells. The antitumor immunity is exerted by infiltrated CD8+ T cells elaborating cytotoxic effectors, like Fas ligand (FasL, CD95L or CD178). As a nuclear factor-kappaB (NF-kappaB)-dependent molecule, Fas is induced by LMP1, and LMP1 enhances Fas-mediated apoptosis, according to our finding of stimulus-dependent apoptosis regulation by LMP1. Data has shown that FasL-mediated cytotoxicity has significant therapeutic effect on EBV-associated nasopharyngeal carcinoma (NPC). Recent reports suggest that mutations affecting the Fas-mediated apoptotic pathway reduce individuals' susceptibility to cancers, but cytokine-targeting therapy which precisely regulates the Fas level on tumor cells could still contribute to enhancement of antitumor immunity in cancer patients.
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| http://dx.doi.org/10.5732/cjc.009.10077 | DOI Listing |
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