ArticleThe Journal of biological chemistry2011
Identification of key amino acid residues that determine the ability of high risk HPV16-E7 to dysregulate major histocompatibility complex class I expression.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 36 citations in OpenAlex.
- Role of hyperthermia in overcoming HPV‑mediated MHC‑Ⅰ downregulation and promoting immune surveillance.International journal of molecular medicine · 2026Article
- Cell-Mediated Immunity Against Human Papillomavirus Infection: From Viral Clearance to Oncogenesis.Viruses · 2026Review
- Downregulation of HLA Class I Expression through HLA-A DNA Methylation Is Associated with Reduced CD8+ T-cell Infiltration in Cervical Cancer.Cancer immunology research · 2026Article
- HIV-associated immune remodeling in cervical cancer: implications for immunotherapy, biomarkers, and trial design.Frontiers in immunology · 2026Review
- Targeting archetypes of viral-driven cancers with immunotherapy: a perspective on immunogenicity within the tumor microenvironment.Frontiers in immunology · 2025Review
- Review
- Tumor Immune Microenvironment in Gynecologic Cancers.Cancers · 2023Review
- Reduced MHC Class I and II Expression in HPV-Negative vs. HPV-Positive Cervical Cancers.Cells · 2022Article
- Article
- Article
- HPV16 E6 gene polymorphisms and the functions of the mutation site in cervical cancer among Uygur ethnic and Han nationality women in Xinjiang, China.Cancer cell international · 2022Article
- The association of cervicovaginal Langerhans cells with clearance of human papillomavirus.Frontiers in immunology · 2022Review
- The Role of the Cervicovaginal and Gut Microbiome in Cervical Intraepithelial Neoplasia and Cervical Cancer.Journal of immunotherapy and precision oncology · 2021Review
- Identification of critical amino acid residues in the regulatory N-terminal domain of PMEL.Scientific reports · 2021Article
- Cervicovaginal Microbiome Factors in Clearance of Human Papillomavirus Infection.Frontiers in oncology · 2021Review
- Evaluation of HPV16 E7 expression in head and neck carcinoma cell lines and clinical specimens.Scientific reports · 2020Article
- Gut microbial diversity and genus-level differences identified in cervical cancer patients versus healthy controls.Gynecologic oncology · 2019Article
- Protecting Tumors by Preventing Human Papilloma Virus Antigen Presentation: Insights from Emerging Bioinformatics Algorithms.Cancers · 2019Review
- Article
- Screening for HPV infection in exfoliated cervical cells of women from different ethnic groups in Yili, Xinjiang, China.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High risk human Papillomavirus (HPV) types are the major causative agents of cervical cancer. Reduced expression of major histocompatibility complex class I (MHC I) on HPV-infected cells might be responsible for insufficient T cell response and contribute to HPV-associated malignancy. The viral gene product required for subversion of MHC I synthesis is the E7 oncoprotein. Although it has been suggested that high and low risk HPVs diverge in their ability to dysregulate MHC I expression, it is not known what sequence determinants of HPV-E7 are responsible for this important functional difference. To investigate this, we analyzed the capability to affect MHC I of a set of chimeric E7 variants containing sequence elements from either high risk HPV16 or low risk HPV11. HPV16-E7, but not HPV11-E7, causes significant diminution of mRNA synthesis and surface presentation of MHC I, which depend on histone deacetylase activity. Our experiments demonstrate that the C-terminal region within the zinc finger domain of HPV-E7 is responsible for the contrasting effects of HPV11- and HPV16-E7 on MHC I. By using different loss- and gain-of-function mutants of HPV11- and HPV16-E7, we identify for the first time a residue variation at position 88 that is highly critical for HPV16-E7-mediated suppression of MHC I. Furthermore, our studies suggest that residues at position 78, 80, and 88 build a minimal functional unit within HPV16-E7 required for binding and histone deacetylase recruitment to the MHC I promoter. Taken together, our data provide new insights into how high risk HPV16-E7 dysregulates MHC I for immune evasion.
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