Role of Toll-like receptors in persistent infection of cervical high-risk human papillomavirus based on "latent pathogen theory".
10.19540/j.cnki.cjcmm.20250109.501
- Author:
Dan-Dan HONG
1
;
Ting-Ting SHANG
2
;
Hong-Yu GUO
1
;
Wen-Ting ZUO
2
;
Rui SUN
1
;
Wen-Wen XU
1
;
Qing-Ling REN
1
Author Information
1. Affiliated Hospital of Nanjing University of Chinese Medicine Nanjing 210029, China Traditional Chinese Medicine Obstetrics and Gynecology Reproductive Clinical Medicine Innovation Center Nanjing 210029, China.
2. Affiliated Hospital of Nanjing University of Chinese Medicine Nanjing 210029, China.
- Publication Type:English Abstract
- Keywords:
Toll-like receptors;
cervical high-risk human papillomavirus;
immune;
latent pathogen
- MeSH:
Humans;
Toll-Like Receptors/genetics*;
Female;
Papillomavirus Infections/genetics*;
Papillomaviridae/immunology*;
Persistent Infection/genetics*;
Uterine Cervical Neoplasms/immunology*;
Animals;
Medicine, Chinese Traditional;
Cervix Uteri/immunology*;
Human Papillomavirus Viruses
- From:
China Journal of Chinese Materia Medica
2025;50(7):1974-1979
- CountryChina
- Language:Chinese
-
Abstract:
Persistent infection with high-risk human papillomavirus(HR-HPV) is the primary etiological factor in cervical lesions and cervical cancer. Toll-like receptors(TLRs), as important pattern recognition receptors of the innate immune system, play a key role in the persistence of cervical HR-HPV infection. The "latent pathogen theory" in traditional Chinese medicine(TCM) holds that latent pathogens have both "latent" and "triggered" characteristics, which closely resemble the persistent infection and latent pathogenic potential of cervical HR-HPV. Guided by the "latent pathogen theory" and using contemporary immunological techniques, this paper explores the bidirectional immunomodulatory effects of TLRs in the persistence of cervical HR-HPV infection and their relationship with latent pathogens. The results indicate that TLRs play a crucial role in immune recognition and modulation. Dysregulation and overactivation of TLRs can induce chronic inflammation, allowing cervical HR-HPV to persist and evade immune detection. TLR dysfunction, coupled with a deficiency in healthy Qi that prevents the expulsion of pathogens, is a critical factor in the pathogenicity of latent pathogens. Restoring healthy Qi to modulate the immune functions of TLRs emerges as an important strategy for clearing cervical HR-HPV infection. By harmonizing the spleen and kidney and regulating immune balance, it is possible to reverse cervical HR-HPV infection, providing a scientific basis for clinical research.
