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在突尼斯宫颈癌患者中,ebv 共感染与 HPV16 基因组完整性之间的相关性。

Correlation between ebv co-infection and HPV16 genome integrity in Tunisian cervical cancer patients.

机构信息

Unit of Immunology Microbiology Environmental and Carcinogenesis (IMEC), Science Faculty of Bizerte, University of Carthage , 7021 Jarzouna, Bizerte , Tunisia.

出版信息

Braz J Microbiol. 2012 Apr;43(2):744-53. doi: 10.1590/S1517-83822012000200039. Epub 2012 Jun 1.

DOI:10.1590/S1517-83822012000200039
PMID:24031886
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3768824/
Abstract

Infection with high risk Human papillomavirus (HR-HPV) is necessary but not sufficient to cause cervical carcinoma. This study explored whether multiple HR-HPV or coinfection with Epstein-Barr virus (EBV) influence the integration status of HPV16 genome. The presence and typing of HPV in a series of 125 cervical specimens were assessed by polymerase chain reaction (PCR) using the specific primers for the HPV L1 region. As for EBV infection, the viral EBNA1 gene was used for its detection through PCR amplification. Disruption of the HPV E2 gene was assessed by amplification of the entire E2 gene with single set of primers, while E2 transcripts were evaluated by a reverse transcription PCR method (RT-PCR). The overall prevalence of HPVDNA was of 81.8% in cervical cancers versus 26.9% in benign lesions. In HPV positive cases, HPV16 and HPV18 were the most prevalent types, followed by HPV types 33, 31. EBV EBNA1 prevalence was statistically more frequent in cervical carcinomas than in benign lesions (29.5%, vs 9.6%; P=0.01). No viral infection was detected in healthy control women. The uninterrupted E2 gene was correlated with the presence of E2 transcripts originating from the HPV episomal forms. It was observed that integration was more common in HPV18 and EBV coinfection. The presence of EBV caused a five-fold [OR= 5; CI= 1.15-21.8; P = 0.04] increase in the risk of HPV16 genome integration in the host genome. This study indicates that EBV infection is acting as a cofactor for induction of cervical cancer by favoring HPVDNA integration.

摘要

高危型人乳头瘤病毒(HR-HPV)感染是导致宫颈癌的必要条件,但不是充分条件。本研究探讨了是否存在多种 HR-HPV 或与 EBV 共同感染会影响 HPV16 基因组的整合状态。通过使用针对 HPV L1 区域的特异性引物的聚合酶链反应(PCR),评估了一系列 125 个宫颈标本中 HPV 的存在和分型。对于 EBV 感染,通过 PCR 扩增检测病毒的 EBNA1 基因。通过使用一组引物扩增整个 E2 基因来评估 HPV E2 基因的破坏情况,同时通过逆转录 PCR 方法(RT-PCR)评估 E2 转录物。在宫颈癌中,HPV DNA 的总体患病率为 81.8%,而良性病变为 26.9%。在 HPV 阳性病例中,HPV16 和 HPV18 是最常见的类型,其次是 HPV 类型 33、31。与良性病变相比,宫颈癌中 EBV EBNA1 的患病率统计学上更高(29.5%,9.6%;P=0.01)。健康对照组妇女未检测到病毒感染。未中断的 E2 基因与源自 HPV episomal 形式的 E2 转录物的存在相关。观察到整合在 HPV18 和 EBV 共同感染中更为常见。EBV 的存在导致 HPV16 基因组整合到宿主基因组中的风险增加五倍[OR=5;CI=1.15-21.8;P=0.04]。本研究表明,EBV 感染作为诱导宫颈癌的协同因子,通过促进 HPV DNA 整合起作用。

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