首页> 外文期刊>Journal of clinical virology: The official publication of the Pan American Society for Clinical Virology >Human papillomavirus HPV-16, 18, 52 and 58 integration in cervical cells of HIV-1-infected women.
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Human papillomavirus HPV-16, 18, 52 and 58 integration in cervical cells of HIV-1-infected women.

机译:人乳头瘤病毒HPV-16、18、52和58整合到HIV-1感染妇女的宫颈细胞中。

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BACKGROUND: Genomic integration of high-risk human papillomavirus into the cellular genome is considered an important event in the pathogenesis of cervical cancer related to the progression from premalignant cervical lesions to invasive cervical carcinoma. OBJECTIVE: This cross-sectional study was aimed to characterize the viral integration of HPV-16, HPV-18, HPV-52 and HPV-58 in cervical cells. STUDY DESIGN: HPV genotypes were determined by PCR and HPV integration by multiplex PCR in HIV-1-infected women without a background of HPV-related pathology. RESULTS: This study included 251 cervical cells samples of consecutive HIV-positive women who were visited between 1999 and 2003. The overall prevalence of HPV infection was 53% (133/251, 95%CI: 47-59%). The most prevalent genotypes were HPV-16 (27%), HPV-33 (15%), HPV-52 (8%) and HPV-58 (8%). The prevalence of abnormal cervical cytology was 33% (83/251, 95%CI: 27-39%). The overall prevalence of HPV integration was 11% (27/251, 95%CI: 7-15%), and the prevalence of HPV-16 integration was 33% (22/67, 95%CI: 22-45%), HPV-18 integration was 30% (3/10, 95%CI: 7-65%) and HPV-52 integration was 10% (2/19, 95%CI: 1-32%). No HPV-58 integration was detected. The percentage of HPV-16 and HPV-18 integration increased with the severity of the cervical lesions, HPV-16 integration was almost 70% and HPV-18 integration was 50% in high-grade squamous intraepithelial lesions. Integration was the most important risk factor associated with cervical dysplasia (OR=30.6, 95%CI: 3.5-270.6). CONCLUSION: HPV integration might represent a good biomarker of the evolution from HPV infection to cervical cancer. Further prospective studies are required to validate our findings.
机译:背景:高风险的人乳头瘤病毒基因组整合到细胞基因组中被认为是子宫颈癌发病过程中的重要事件,与从癌前宫颈病变发展为浸润性子宫颈癌有关。目的:这项横断面研究旨在表征宫颈细胞中HPV-16,HPV-18,HPV-52和HPV-58的病毒整合。研究设计:在没有HPV相关病理学背景的HIV-1感染妇女中,通过PCR和多重PCR整合测定HPV基因型。结果:这项研究包括1999年至2003年间连续访问的251例HIV阳性女性宫颈细胞样本。HPV感染的总体患病率为53%(133 / 251,95%CI:47-59%)。最流行的基因型是HPV-16(27%),HPV-33(15%),HPV-52(8%)和HPV-58(8%)。宫颈细胞学异常的患病率为33%(83/251,95%CI:27-39%)。 HPV整合的总体患病率为11%(27/251,95%CI:7-15%),HPV-16整合的患病率为33%(22/67,95%CI:22-45%), HPV-18整合率为30%(3/10,95%CI:7-65%),HPV-52整合率为10%(2/19,95%CI:1-32%)。未检测到HPV-58集成。 HPV-16和HPV-18整合的百分比随宫颈病变的严重程度而增加,在高度鳞状上皮内病变中,HPV-16整合几乎为70%,HPV-18整合为50%。整合是与宫颈发育不良相关的最重要的危险因素(OR = 30.6,95%CI:3.5-270.6)。结论:HPV整合可能代表了从HPV感染到宫颈癌的良好生物标志。需要进一步的前瞻性研究来验证我们的发现。

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