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Endogenous retroviruses and response to immune checkpoint inhibitors: mechanisms, clinical evidence, and therapeutic

Fanyuan Wu1, Quezhu Danzeng2, Runxi Wu3

  • 1Department of Hematology and Oncology, The Second Hospital of Jilin University, Changchun, China.

Frontiers in Immunology
|June 5, 2026
PubMed

Insights

Endogenous retroviruses (ERVs) activation in cancer boosts anti-tumor immunity and PD-L1 expression, potentially serving as biomarkers for immunotherapy response. Strategies to induce ERVs may enhance cancer treatment efficacy.

Area of Science:

  • Oncology
  • Immunology
  • Genomics

Background:

  • Endogenous retroviruses (ERVs) are genomic remnants that can be reactivated in cancer.
  • Reactivated ERVs produce double-stranded RNA (dsRNA) and proteins, mimicking viral infection.
  • This viral mimicry triggers innate immune pathways, including MDA5/RIG-I and TLR3 signaling.

Purpose of the Study:

  • To investigate the role of ERV reactivation in cancer immunity.
  • To explore ERV signatures as biomarkers for immunotherapy response.
  • To evaluate therapeutic strategies involving ERV induction.

Main Methods:

  • Analysis of ERV reactivation in cancer via DNA hypomethylation and chromatin remodeling.
  • Assessment of dsRNA sensing by MDA5/RIG-I and TLR3, activating MAVS/TRIF signaling.
  • Evaluation of downstream effects on interferon production, antigen presentation, immune cell recruitment, and tumor microenvironment modulation.

Main Results:

  • ERV reactivation enhances antigen processing and MHC-I presentation.
  • It promotes recruitment of effector lymphocytes (CXCR3+) and dendritic cell activation.
  • ERV signatures show promise as biomarkers for immune checkpoint inhibitor (ICI) response, independent of PD-L1 or tumor mutational burden.

Conclusions:

  • ERV reactivation converts immune-cold tumors into immune-active states.
  • ERV signatures can enable patient stratification for ICI therapy.
  • Therapeutic induction of ERVs may sensitize tumors to ICIs, but requires further validation and safety assessment.
Keywords:
endogenous retrovirusesepigenetic regulationimmune checkpoint inhibitorstumor microenvironmentviral mimicry

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