Altered immune responses in HR-HPV infected women
5 affiliations
- 1Subdirección de Desarrollo de Aplicaciones Clínicas, Instituto Nacional de Medicina Genómica , ,
- 2Centro de Investigación Sobre Enfermedades Infecciosas, Instituto Nacional de Salud Pública , , ,
- 3Subdirección de Investigación Básica, Instituto Nacional de Cancerología , ,
- 4Universidad de Guadalajara, Centro Universitario de Ciencias de la Salud, Departamento de Fisiología , , ,
- 5Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública , , ,
Abstract
Persistent infection with high-risk human papillomavirus (HR-HPV) is the primary cause of cervical cancer (CC). However, most HPV infections are transient and are cleared by effective host immune responses. Therefore, understanding the mechanisms that allow viral persistence and immune escape is critical to explaining why only a subset of women develops cervical lesions and invasive cancer. Although cervical cancer is largely preventable through vaccination and screening, it remains a major cause of cancer-related morbidity and mortality among women worldwide, with a disproportionate burden in low- and middle-income countries. This significant disparity underscores the ongoing inequities in access to HPV vaccination, screening, and timely treatment, which hinder the World Health Organization aim to eliminate cervical cancer as a public health concern by 2030. This narrative review examines how viral, host, and microenvironmental factors interact to promote HR-HPV persistence and cervical cancer development, with particular attention to evidence from Mexican women. HR-HPV can evade immune surveillance by interfering with innate immune recognition, interferon signaling, antigen presentation, and cytotoxic lymphocyte activity. These alterations are compounded by cervicovaginal dysbiosis, immunosuppressive cytokines, regulatory-cell expansion, host genetic variation, and altered microRNA expression. Together, these interconnected processes impair viral clearance and create conditions that favor the progression of cervical lesions to invasive cancer. A comprehensive understanding of these mechanisms may facilitate the identification of biomarkers of HPV persistence and disease progression, while supporting the development of more effective immunotherapeutic strategies and precision prevention approaches, particularly for populations disproportionately affected by cervical cancer.
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BibTeX
@article{martinezcampos2026altered,
title = {{Altered immune responses in HR-HPV infected women}},
author = {Cecilia Martínez-Campos and Kirvis Torres-Poveda and Marcela Lizano and Susana del Toro-Arreola and Carla O. Contreras-Ochoa and Margarita Bahena-Román and Víctor Hugo Bermúdez-Morales and Oscar Peralta-Zaragoza and Alfredo Lagunas-Martínez and Abrahan Ramírez-González and Jorge Cime-Castillo and Aurelio Cruz-Valdez and Vicente Madrid-Marina},
journal = {Frontiers in medicine},
year = {2026},
month = oct,
doi = {10.3389/fmed.2026.1986999},
url = {https://europepmc.org/article/PMC/PMC13717847},
note = {CC BY},
}
RIS
TY - JOUR
TI - Altered immune responses in HR-HPV infected women
AU - Cecilia Martínez-Campos
AU - Kirvis Torres-Poveda
AU - Marcela Lizano
AU - Susana del Toro-Arreola
AU - Carla O. Contreras-Ochoa
AU - Margarita Bahena-Román
AU - Víctor Hugo Bermúdez-Morales
AU - Oscar Peralta-Zaragoza
AU - Alfredo Lagunas-Martínez
AU - Abrahan Ramírez-González
AU - Jorge Cime-Castillo
AU - Aurelio Cruz-Valdez
AU - Vicente Madrid-Marina
PY - 2026
DA - 2026/10/15
JO - Frontiers in medicine
DO - 10.3389/fmed.2026.1986999
UR - https://europepmc.org/article/PMC/PMC13717847
AB - Persistent infection with high-risk human papillomavirus (HR-HPV) is the primary cause of cervical cancer (CC). However, most HPV infections are transient and are cleared by effective host immune responses. Therefore, understanding the mechanisms that allow viral persistence and immune escape is critical to explaining why only a subset of women develops cervical lesions and invasive cancer. Although cervical cancer is largely preventable through vaccination and screening, it remains a major cause of cancer-related morbidity and mortality among women worldwide, with a disproportionate burden in low- and middle-income countries. This significant disparity underscores the ongoing inequities in access to HPV vaccination, screening, and timely treatment, which hinder the World Health Organization aim to eliminate cervical cancer as a public health concern by 2030. This narrative review examines how viral, host, and microenvironmental factors interact to promote HR-HPV persistence and cervical cancer development, with particular attention to evidence from Mexican women. HR-HPV can evade immune surveillance by interfering with innate immune recognition, interferon signaling, antigen presentation, and cytotoxic lymphocyte activity. These alterations are compounded by cervicovaginal dysbiosis, immunosuppressive cytokines, regulatory-cell expansion, host genetic variation, and altered microRNA expression. Together, these interconnected processes impair viral clearance and create conditions that favor the progression of cervical lesions to invasive cancer. A comprehensive understanding of these mechanisms may facilitate the identification of biomarkers of HPV persistence and disease progression, while supporting the development of more effective immunotherapeutic strategies and precision prevention approaches, particularly for populations disproportionately affected by cervical cancer.
SN - 2296-858X
ER -