ArticlePloS one2014
E2 proteins of high risk human papillomaviruses down-modulate STING and IFN-κ transcription in keratinocytes.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 96 citations in OpenAlex.
- Virus-mediated immunosuppression in head and neck cancer.Oncogene · 2025Review
- The role of cGAS-STING signaling in HPV infection and HPV-related cancers.Frontiers in immunology · 2025Review
- Human papillomavirus E2 proteins suppress innate antiviral signaling pathways.Frontiers in immunology · 2025Article
- Review
- A Critical Role for IFN-β Signaling for IFN-κ Induction in Keratinocytes.Frontiers in lupus · 2024Article
- The cGAS-STING pathway and female reproductive system diseases.Frontiers in immunology · 2024Review
- Bioinformatics analysis of immune characteristics in tumors with alternative carcinogenesis pathways induced by human papillomaviruses.Virology journal · 2023Article
- Plasmacytoid Dendritic Cells, the Expression of the Stimulator of Interferon Genes Protein (STING) and a Possible Role of Th17 Immune Response in Cervical Lesions Mediated by Human Papillomavirus.Indian journal of microbiology · 2023Article
- Human papillomaviruses: Knowns, mysteries, and unchartered territories.Journal of medical virology · 2023Review
- Human papillomavirus E5 suppresses immunity via inhibition of the immunoproteasome and STING pathway.Cell reports · 2023Article
- Review
- Review
- Epigenetically suppressed tumor cell intrinsic STING promotes tumor immune escape.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Crosstalk between cGAS-STING pathway and autophagy in cancer immunity.Frontiers in immunology · 2023Review
- Alteration of the IFN-Pathway by Human Papillomavirus Proteins: Antiviral Immune Response Evasion Mechanism.Biomedicines · 2022Review
- Review
- Human Beta Papillomavirus Type 8 E1 and E2 Proteins Suppress the Activation of the RIG-I-Like Receptor MDA5.Viruses · 2022Article
- High-Risk Mucosal Human Papillomavirus 16 (HPV16) E6 Protein and Cutaneous HPV5 and HPV8 E6 Proteins Employ Distinct Strategies To Interfere with Interferon Regulatory Factor 3-Mediated Beta Interferon Expression.Journal of virology · 2022Article
- High-Risk Human Papillomavirus and Epstein-Barr Virus Coinfection: A Potential Role in Head and Neck Carcinogenesis.Biology · 2021Review
- Virus-Induced Tumorigenesis and IFN System.Biology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the early stages of human papillomavirus (HPV) infection, the viral proteins elicit specific immune responses that can participate to regression of ano-genital lesions. HPV E6 protein for instance can reduce type I interferon (IFN) including IFN-κ that is involved in immune evasion and HPV persistence. To evaluate the role of E2 protein in innate immunity in HPV16-associated cervical lesions, genome-wide expression profiling of human primary keratinocytes (HPK) transduced by HPV16 E2 was investigated using microarrays and innate immunity associated genes were specifically analyzed. The analyses showed that the expression of 779 genes was modulated by HPV16E2 and 92 of them were genes associated with innate immunity. Notably IFN-κ and STING were suppressed in HPK expressing the E2 proteins of HPV16 or HPV18 and the trans-activation amino-terminal domain of E2 was involved in the suppressive effect. The relationship between STING, IFN-κ and interferon stimulated genes (ISGs) in HPK was confirmed by gene silencing and real time PCR. The expression of STING and IFN-κ were further determined in clinical specimens by real time PCR. STING and IFN-κ were down-modulated in HPV positive low grade squamous intraepithelial lesions compared with HPV negative controls. This study demonstrates that E2 proteins of high risk HPV reduce STING and IFN-κ transcription and its downstream target genes that might be an immune evasion mechanism involved in HPV persistence and cervical cancer development.
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Registered trials
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