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Updated: May 29, 2025

Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo
Published on: January 7, 2019
Exploring viral mimicry combined with epigenetics and tumor immunity: new perspectives in cancer therapy
Ruirui Wang1, Xin Dong2, Xiongjian Zhang1
1Department of Radiology, The Third Xiangya Hospital of Central South University. Tongzipo Road 138, Changsha, Hunan, People's Republic of China.
Abstract:
Viral mimicry refers to an active antiviral response triggered by the activation of endogenous retroviruses (ERVs), usually manifested by the formation of double-stranded RNA (dsRNA) and activation of the cellular interferon response, which activates the immune system and produces anti-tumor effects. Epigenetic studies have shown that epigenetic modifications (e.g. DNA methylation, histone modifications, etc.) play a crucial role in tumorigenesis, progression, and treatment resistance. Particularly, alterations in DNA methylation may be closely associated with the suppression of ERVs expression, and treatment by demethylation may restore ERVs activity and thus strengthen the tumor immune response. Therefore, we propose that viral mimicry can induce immune responses in the tumor microenvironment by activating the expression of ERVs, and that epigenetic alterations may play a key regulatory role in this process. In this paper, we review the intersection of viral mimicry, epigenetics and tumor immunotherapy, and explore the possible interactions and synergistic effects among the three, aiming to provide a new theoretical basis and potential strategies for cancer immunotherapy.
Insights
Viral mimicry, triggered by endogenous retroviruses (ERVs), enhances anti-tumor immunity. Epigenetic alterations regulate ERV expression, offering new cancer immunotherapy strategies by restoring ERV activity.
Area of Science:
- Immunology
- Epigenetics
- Oncology
Background:
- Viral mimicry involves endogenous retroviruses (ERVs) activating immune responses.
- Epigenetic modifications critically influence cancer development and treatment resistance.
- DNA methylation alterations are linked to suppressed ERV expression in tumors.
Purpose of the Study:
- To review the interplay between viral mimicry, epigenetics, and tumor immunotherapy.
- To explore synergistic effects for novel cancer treatment strategies.
- To provide a theoretical basis for enhancing tumor immune responses.
Main Methods:
- Literature review of viral mimicry mechanisms.
- Analysis of epigenetic regulation in cancer.
- Exploration of ERV activation in tumor microenvironments.
Main Results:
- Viral mimicry, via ERVs, can stimulate anti-tumor immune responses.
- Epigenetic modifications, particularly DNA methylation, regulate ERV expression.
- Demethylation therapies may reactivate ERVs, boosting anti-tumor immunity.
Conclusions:
- Viral mimicry and epigenetics are key regulators of tumor immunity.
- Targeting ERV expression through epigenetic manipulation is a promising immunotherapy approach.
- Understanding these interactions can lead to more effective cancer treatments.
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