The seroepidemiology of genital human papillomavirus (HPV) and incident cervical squamous intraepithelial lesions (SIL) was studied in subjects selected from a large cohort monitored for the development of SIL. Serum IgG and IgA responses to 10 epitopes derived from HPV were measured in 21 incident cases of SIL and 56 matched controls. Cases showed elevated antibody (i.e., IgG and/or IgA) seroprevalence to 245:16, a peptide antigen derived from the E2 open reading frame of HPV 16 (OR = 5.76; 95% CI: 1.24, 26.81). The type of HPV DNA detected in cervical lavage specimens had no effect on this relationship. Multivariate analysis also showed that IgG to 245:6, an analogous peptide derived from HPV 6, was negatively associated with SIL (OR = 0.12; 95% CI: 0.02, 0.77). No other antibody responses tested were associated with SIL. Furthermore, no antibody responses were positively associated with detection of HPV DNA in women without SIL. We conclude that incident SIL is positively associated with antibody to an epitope derived from the E2 region of HPV 16, and negatively associated with antibody to an analogous peptide derived from HPV 6. The seroepidemiology of incident SIL appears different from that of cervical HPV infection in the absence of SIL.
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http://dx.doi.org/10.1089/vim.1994.7.169 | DOI Listing |
J Med Virol
February 2025
Department of Medical Technology, Faculty of Health Sciences, Kyorin University, Tokyo, Japan.
In cervical cancer screening, cytology is used as a triage test to refer high-risk human papillomavirus (HR-HPV)-positive women for colposcopy, but its accuracy is inadequate. The present study aimed to demonstrate that the presence of atypical cells with large vacuoles in the cytoplasm of parabasal cells, referred to as vacuolated parabasal cells (VPCs), which are observed in the Pap smears of HPV-positive women, is associated with specific HPV genotypes. Among 2175 patients, 310 with a single HR-HPV infection and cytological diagnosis of high-grade squamous intraepithelial lesions (HSIL) or atypical squamous cells not excluding HSIL (ASC-H) were included, of which 86 were infected with HPV16.
View Article and Find Full Text PDFViruses
December 2024
Department of Rehabilitation and Regenerative Medicine, College of Physicians and Surgeons, Columbia University, HHSC-1518, 701 W. 168th Street, New York, NY 10032, USA.
This study explores the effects of plant compounds on human papillomavirus (HPV)-induced W12 cervical precancer cells and bioelectric signaling. The aim is to identify effective phytochemicals, both individually and in combination, that can prevent and treat HPV infection and HPV associated cervical cancer. Phytochemicals were tested using growth inhibition, combination, gene expression, RT PCR, and molecular docking assays.
View Article and Find Full Text PDFCancers (Basel)
January 2025
Head and Neck Oncology Group, Centre for Host Microbiome Interaction, King's College London, Hodgkin Building, London SE1 1UL, UK.
Background: Cancer-associated fibroblasts have been reported to play a central role in driving cancer progression, promoting metastasis, and conferring resistance to therapy in HNSCC.
Methods: Indirect and direct co-culture models of HPV-positive and HPV-negative HNSCC cells with fibroblasts were developed to study the effect of fibroblasts on cancer cells. ELISA was used to measure IL-6 secretion in these models.
Tzu Chi Med J
December 2024
Department of Obstetrics and Gynecology, College of Medicine, University of Babylon, Hilla, Iraq.
The most common STD that triggers cervical cancer is the human papillomavirus. More than 20 types of human papillomavirus (HPV) can induce uterine cervical cancer. Almost all women acquire genital HPV infection soon after their first intercourse, with most of them clearing the virus within 3 years.
View Article and Find Full Text PDFFunct Integr Genomics
January 2025
Department of Oncology, the First People's Hospital of Qujing City/the Qujing Affiliated Hospital of Kunming Medical University, 1 Yuanlin Road, Qujing, Yunnan, China.
Background: T cells are involved in every stage of tumor development and significantly influence the tumor microenvironment (TME). Our objective was to assess T-cell marker gene expression profiles, develop a predictive risk model for human papilloma virus (HPV)-negative oral squamous cell carcinoma (OSCC) utilizing these genes, and examine the correlation between the risk score and the immunotherapy response.
Methods: We acquired scRNA-seq data for HPV-negative OSCC from the GEO datasets.
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