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中文摘要
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异嗜性鼠白血病病毒相关病毒(XMRV)首先在前列腺癌患者的前列腺组织中鉴定。随后对该病毒流行的研究产生了不一致的结果,使得该病毒与前列腺癌之间的联系尚不清楚。我们应用实时定量PCR检测和两个良好控制的免疫组化(IHC)检测XMRV在新鲜获得的和存档的组织标本。我们的实时PCR检测可靠地检测来自22Rv1细胞(一种XMRV感染的细胞系)的单细胞基因组DNA(gDNA)中的XMRV DNA,即使在存在大量过量未感染细胞gDNA的情况下。我们的免疫组化检测使用了两种特异性针对鼠白血病病毒p30CA和gp70SU的兔多克隆抗血清。两种抗血清均显示出22Rv1细胞和XMRV转染细胞的强免疫染色,但未染色许多未感染的细胞系。我们通过实时PCR检测了161份前列腺肿瘤来源的DNA样本,并通过IHC检测了596份前列腺肿瘤组织样本。我们的肿瘤组织富集了具有高Gleason评分的病例(例如,小于或等于7)并且包括许多转移性病变。我们还通过IHC检测了452例含有各种良性病变的前列腺组织。我们没有在任何测试样品中检测到XMRV。研究结果表明,在北美男性的良性和恶性前列腺组织中,XMRV的患病率极低或不存在。
英文摘要
Xenotropic Murine Leukemia Virus Related Virus (XMRV) was first identified in prostate tissues from prostate cancer patients. Subsequent studies on the prevalence of the virus have produced inconsistent results, leaving the link between the virus and prostate cancer unclear. We applied a quantitative real-time PCR assay and two well-controlled immunohistochemistry (IHC) assays for the detection of XMRV in freshly obtained and archival tissue specimens. Our real-time PCR assay reliably detected XMRV DNA from a single cells worth of genomic DNA (gDNA) from 22Rv1 cells, an XMRV-infected cell line, even in the presence of a vast excess of uninfected cell gDNA. Our IHC assays utilized two rabbit polyclonal antisera specific for murine leukemia virus, p30CA and gp70SU. Both antisera showed robust immunostaining of 22Rv1 cells and XMRV-transfected cells, but did not stain a number of uninfected cell lines. We tested 161 prostate tumor-derived DNA samples by real-time PCR and 596 prostate tumor tissue specimens by IHC. Our tumor tissues were enriched for cases with high Gleason score (e.g., less than or equal to 7) and included a number of metastatic lesions. We also tested 452 prostate tissues containing a variety of benign pathologies by IHC. We did not detect XMRV in any of the samples tested. The findings suggest an extremely low prevalence, or absence, of XMRV in benign and malignant prostate tissues in men living in North America.
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Mechanisms in Retroviral Replication and Pathogenesis
Retrovirus Assembly and Maturation
MECHANISMS IN RETROVIRAL REPLICATION AND PATHOGENESIS
Retrovirus Assembly and Maturation
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