Strickler H D, Viscidi R, Escoffery C, Rattray C, Kotloff K L, Goldberg J, Manns A, Rabkin C, Daniel R, Hanchard B, Brown C, Hutchinson M, Zanizer D, Palefsky J, Burk R D, Cranston B, Clayman B, Shah K V
Viral Epidemiology Branch, National Cancer Institute, NIH, Bethesda, Maryland, USA.
J Med Virol. 1999 Sep;59(1):60-5. doi: 10.1002/(sici)1096-9071(199909)59:1<60::aid-jmv10>3.0.co;2-8.
Evidence from several sources has suggested that adeno-associated virus (AAV) infection might protect against cervical cancer, in part, by interfering with human papillomavirus (HPV)-induced tumorigenesis. Detection of AAV type 2 (AAV-2) DNA in cervical tissues has been reported. However, there have been few in vivo studies of women with cervical HPV infection or neoplasia, and these have reported inconsistent results. Therefore, we used polymerase chain reaction (PCR) assays targeted to the AAV-2 rep and cap genes to test tissue specimens from women in an epidemiological study of cervical neoplasia in Jamaica. We tested 105 women with low-grade cervical intraepithelial neoplasia (CIN-1), 92 women with CIN-3/carcinoma in situ or invasive cancer (CIN-3/CA), and 94 normal subjects. PCR amplification of human beta-globin DNA was found in almost all cervical specimens, indicating that these materials were adequate for PCR testing. The prevalence of HPV DNA, determined by HPV L1 consensus primer PCR was, as expected, strongly associated with presence and grade of neoplasia. Each of the AAV PCR assays detected as few as 10 copies of the virus genome. However, none of the 291 cervical specimens from Jamaican subjects tested positive for AAV DNA. Negative AAV PCR results were also obtained in tests of cervical samples from 79 university students in the United States. Exposure to AAV was assessed further by serology. Using a whole virus AAV-2 sandwich enzyme-linked immunosorbent assay, we found no relationship between AAV antibodies and presence or grade of neoplasia in either the Jamaican study subjects or women enrolled in a U.S. cervical cancer case (n = 74) -control (n = 77) study. Overall, the data provide no evidence that AAV infection plays a role in cervical tumorigenesis or that AAV commonly infects cervical epithelial cells.
来自多个来源的证据表明,腺相关病毒(AAV)感染可能部分通过干扰人乳头瘤病毒(HPV)诱导的肿瘤发生来预防宫颈癌。已有报道在宫颈组织中检测到2型腺相关病毒(AAV-2)DNA。然而,针对宫颈HPV感染或瘤变女性的体内研究较少,且这些研究报告的结果并不一致。因此,在牙买加一项关于宫颈瘤变的流行病学研究中,我们使用针对AAV-2 rep和cap基因的聚合酶链反应(PCR)检测法来检测女性的组织标本。我们检测了105名患有低度宫颈上皮内瘤变(CIN-1)的女性、92名患有CIN-3/原位癌或浸润癌(CIN-3/CA)的女性以及94名正常受试者。几乎在所有宫颈标本中都发现了人β-珠蛋白DNA的PCR扩增,表明这些材料足以进行PCR检测。正如预期的那样,通过HPV L1共识引物PCR测定的HPV DNA患病率与瘤变的存在和分级密切相关。每种AAV PCR检测法都能检测到低至10个拷贝的病毒基因组。然而,来自牙买加受试者的291份宫颈标本中没有一份AAV DNA检测呈阳性。在美国79名大学生的宫颈样本检测中也得到了AAV PCR阴性结果。通过血清学进一步评估了AAV暴露情况。使用全病毒AAV-2夹心酶联免疫吸附测定法,我们发现在牙买加研究对象或参与美国宫颈癌病例(n = 74)-对照(n = 77)研究的女性中,AAV抗体与瘤变的存在或分级之间没有关系。总体而言,这些数据没有提供证据表明AAV感染在宫颈肿瘤发生中起作用,也没有表明AAV通常感染宫颈上皮细胞。