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肛门上皮病变中的人乳头瘤病毒类型受人类免疫缺陷病毒影响。

Human papillomavirus type in anal epithelial lesions is influenced by human immunodeficiency virus.

作者信息

Unger E R, Vernon S D, Lee D R, Miller D L, Sharma S, Clancy K A, Hart C E, Reeves W C

机构信息

Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Ga., USA.

出版信息

Arch Pathol Lab Med. 1997 Aug;121(8):820-4.

PMID:9278609
Abstract

BACKGROUND AND OBJECTIVE

Infection with human immunodeficiency virus (HIV) increases the risk for human papillomavirus (HPV)-associated genital neoplasia. Human immunodeficiency virus-infected patients also have higher rates of treatment failure and more rapid neoplastic progression. Impaired immune function does not entirely explain these clinical observations. This pilot project was designed to investigate the hypothesis that HIV infection is associated with changes in HPV type and integration within anogenital lesions that could explain the increased risk of neoplastic progression.

METHODS

Anal neoplastic lesions from patients with and without HIV infection were analyzed for the presence, type, and integration status of HPV by colorimetric in situ hybridization. Tissue localization of HIV was evaluated by p24 immunohistochemistry and HIV-1 DNA polymerase chain reaction. Results for matched histology were compared for the two patient groups.

RESULTS

For all lesions, the presence of high-risk HPV types and multiple HPV types was strongly associated with HIV infection (P = .003 and .0003, respectively). For lesions with matched histology there was no association of HPV integration with HIV status. Tissue localization of HIV did not significantly influence HPV type or integration.

CONCLUSIONS

The presence of high-risk HPV types and multiple types within low-grade lesions may explain the increased risk of neoplastic progression in HIV patients. Colocalization of HIV and HPV does not appear to be required for this effect. There is no evidence that HPV integration is influenced by HIV infection.

摘要

背景与目的

感染人类免疫缺陷病毒(HIV)会增加患人乳头瘤病毒(HPV)相关生殖器肿瘤的风险。HIV感染患者的治疗失败率也更高,肿瘤进展更快。免疫功能受损并不能完全解释这些临床观察结果。本试点项目旨在研究以下假设:HIV感染与HPV类型变化以及肛门生殖器病变中的整合有关,这可以解释肿瘤进展风险增加的原因。

方法

通过比色原位杂交分析有无HIV感染患者的肛门肿瘤病变中HPV的存在、类型和整合状态。通过p24免疫组织化学和HIV-1 DNA聚合酶链反应评估HIV的组织定位。比较两组患者匹配组织学的结果。

结果

对于所有病变,高危HPV类型的存在和多种HPV类型与HIV感染密切相关(分别为P = .003和.0003)。对于组织学匹配的病变,HPV整合与HIV状态无关。HIV的组织定位对HPV类型或整合没有显著影响。

结论

低级别病变中高危HPV类型和多种类型的存在可能解释了HIV患者肿瘤进展风险增加的原因。这种效应似乎不需要HIV和HPV共定位。没有证据表明HPV整合受HIV感染影响。

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