Clinical study on the pathogenic risks of different genotypes of high-risk HPV infection and multiple infections.

IF 3.2 2区 医学 Q3 IMMUNOLOGY
Meiyu Song, Minhong Mao, Huirong Zhao, Chen Chen
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引用次数: 0

Abstract

Objective: To investigate the oncogenic risks of distinct high-risk human papillomavirus (HR-HPV) genotypes and whether multiple infections exacerbate pathogenicity, with analysis of age stratification and viral load impact.

Methods: Clinical and pathological data from 2,525 patients undergoing colposcopy-directed biopsy for cervical abnormalities (2020-2023) were analyzed. HPV genotyping (18 types) and viral load quantification (Ct-values) were performed using PCR-membrane hybridization. Histopathology (CC/LSIL/HSIL/SCC) was evaluated by blinded experts. Statistical analyses included age stratification (< 35 vs. ≥35 years) and multivariate adjustment for viral load (Ct ≤ 30).

Result: HR-HPV single-type infections predominated (1,774 cases, 70.26%), with genotype distribution: 16 (17.98%), 52 (10.50%), 58 (7.88%), 53 (4.63%), and 18 (4.55%). Multiple infections occurred in 474 cases (18.77%). Versus HPV-negative/low-risk controls, the highest pathogenic risks were: type 16 (OR = 7.96, 95% CI:5.41-11.71), type 58 (OR = 5.80, 95% CI:3.75-8.99), multiple infections (OR = 5.02, 95% CI:3.42-7.37), type 18 (OR = 4.86, 95% CI:2.95-8.02), and type 35 (OR = 4.07, 95% CI:1.82-9.10) (all P = 0.001). Age ≥ 35 years independently increased HSIL + risk (OR = 2.16, 95% CI:1.62-2.88, P = 0.001), with HPV16/18/35 showing significantly higher ORs in this group. High viral load (Ct ≤ 30) independently predicted HSIL + progression (OR = 2.98, 95% CI:1.92-4.63, P = 0.001). Multiple infections did not increase risk for genotypes 16/18/33/35/52/56/58/68 versus single infections, except for HPV51 (P = 0.01).

Conclusion: Genotype 16 demonstrates the strongest oncogenic potential, with pathogenic hierarchy: 16 > 58 > 18 > 35. Multiple infections do not synergistically increase risk for dominant genotypes. Age ≥ 35 years and high viral load (Ct ≤ 30) independently elevate cervical lesion severity, supporting their integration into risk-stratified screening protocols.

Clinical trial number: Not applicable.

Abstract Image

Abstract Image

不同基因型高危HPV感染及多发感染致病风险的临床研究。
目的:探讨不同高危型人乳头瘤病毒(HR-HPV)基因型的致瘤风险及多次感染是否会加重致病性,并分析其年龄分层和病毒载量的影响。方法:分析2020-2023年2525例经阴道镜指导下宫颈异常活检患者的临床和病理资料。采用pcr -膜杂交技术进行HPV基因分型(18型)和病毒载量定量(ct值)。组织病理学(CC/LSIL/HSIL/SCC)由盲法专家评估。结果:HR-HPV单型感染以1774例(70.26%)为主,基因型分布分别为16例(17.98%)、52例(10.50%)、58例(7.88%)、53例(4.63%)、18例(4.55%)。多发感染474例(18.77%)。与hpv阴性/低风险对照组相比,最高致病风险为:16型(OR = 7.96, 95% CI:5.41-11.71)、58型(OR = 5.80, 95% CI:3.75-8.99)、多重感染(OR = 5.02, 95% CI:3.42-7.37)、18型(OR = 4.86, 95% CI:2.95-8.02)和35型(OR = 4.07, 95% CI:1.82-9.10)(均P = 0.001)。年龄≥35岁独立增加HSIL +风险(OR = 2.16, 95% CI:1.62-2.88, P = 0.001), HPV16/18/35组的OR值显著高于HPV16/18/35组。高病毒载量(Ct≤30)独立预测HSIL +进展(OR = 2.98, 95% CI:1.92-4.63, P = 0.001)。除HPV51外,多次感染与单次感染相比,16/18/33/35/52/56/58/68基因型的风险均未增加(P = 0.01)。结论:基因型16表现出最强的致癌潜力,其致病等级为:16 > 58 > 18 > 35。多重感染不会协同增加显性基因型的风险。年龄≥35岁和高病毒载量(Ct≤30)独立提高宫颈病变严重程度,支持将其纳入风险分层筛查方案。临床试验号:不适用。
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来源期刊
Infectious Agents and Cancer
Infectious Agents and Cancer ONCOLOGY-IMMUNOLOGY
CiteScore
5.80
自引率
2.70%
发文量
54
期刊介绍: Infectious Agents and Cancer is an open access, peer-reviewed online journal that encompasses all aspects of basic, clinical, epidemiological and translational research providing an insight into the association between chronic infections and cancer. The journal welcomes submissions in the pathogen-related cancer areas and other related topics, in particular: • HPV and anogenital cancers, as well as head and neck cancers; • EBV and Burkitt lymphoma; • HCV/HBV and hepatocellular carcinoma as well as lymphoproliferative diseases; • HHV8 and Kaposi sarcoma; • HTLV and leukemia; • Cancers in Low- and Middle-income countries. The link between infection and cancer has become well established over the past 50 years, and infection-associated cancer contribute up to 16% of cancers in developed countries and 33% in less developed countries. Preventive vaccines have been developed for only two cancer-causing viruses, highlighting both the opportunity to prevent infection-associated cancers by vaccination and the gaps that remain before vaccines can be developed for other cancer-causing agents. These gaps are due to incomplete understanding of the basic biology, natural history, epidemiology of many of the pathogens that cause cancer, the mechanisms they exploit to cause cancer, and how to interrupt progression to cancer in human populations. Early diagnosis or identification of lesions at high risk of progression represent the current most critical research area of the field supported by recent advances in genomics and proteomics technologies.
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