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潜伏性EB病毒感染在免疫增生性小肠疾病的发病机制中不太可能发生。

Latent Epstein-Barr virus infection is an unlikely event in the pathogenesis of immunoproliferative small intestinal disease.

作者信息

Baddoura F K, Unger E R, Mufarrij A, Nassar V H, Zaki S R

机构信息

Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia.

出版信息

Cancer. 1994 Sep 15;74(6):1699-705. doi: 10.1002/1097-0142(19940915)74:6<1699::aid-cncr2820740610>3.0.co;2-7.

DOI:10.1002/1097-0142(19940915)74:6<1699::aid-cncr2820740610>3.0.co;2-7
PMID:8082070
Abstract

BACKGROUND

The observed seasonal and geographic variations in the incidence of immunoproliferative small intestinal disease (IPSID) suggest that environmental factors contribute to its pathogenesis. One such environmental factor, the Epstein-Barr virus (EBV), has been associated with other B-cell lymphoproliferative disorders.

METHODS

IPSID tissues obtained at the time of initial diagnosis were retrieved from the American University of Beirut pathology archives (1972-1983) and examined for EBV genetic information by colorimetric in situ hybridization (ISH) and polymerase chain reaction (PCR). Eight patients were identified, four of whom also had serologic and immunohistochemical evidence of alpha-heavy chain disease. Thirteen tissue samples from these eight patients were available for study: eight were intestinal and five were nodal. Non-Hodgkin's B-cell lymphoma cases (nine) were randomly selected from the same archive to serve as a control for EBV in that geographic location. The ISH method used a probe to the "W" repetitive region of EBV, with the human placental DNA probe as a control for sample preparation. The PCR method amplified a 110 base pair region in the long internal direct repeat with amplification of beta-actin as control for DNA preservation. Both assays used formalin fixed paraffin embedded Raji cells as a positive control.

RESULTS

Neither ISH nor PCR demonstrated EBV in any of the eight patients with IPSID: The results for one of seven control blocks with adequate DNA preservation were positive when PCR was used but were negative when ISH was used.

CONCLUSIONS

These findings do not support a role for EBV in the induction of B-cell proliferation in IPSID:

摘要

背景

免疫增殖性小肠疾病(IPSID)发病率呈现出季节性和地理性变化,这表明环境因素在其发病机制中起作用。一种这样的环境因素,即爱泼斯坦-巴尔病毒(EBV),已与其他B细胞淋巴增殖性疾病相关。

方法

从贝鲁特美国大学病理档案库(1972 - 1983年)中获取初诊时的IPSID组织,并通过比色原位杂交(ISH)和聚合酶链反应(PCR)检测EBV基因信息。共鉴定出8例患者,其中4例还具有α重链病的血清学和免疫组化证据。这8例患者的13份组织样本可用于研究:8份为肠道样本,5份为淋巴结样本。从同一档案库中随机选取9例非霍奇金B细胞淋巴瘤病例作为该地理位置EBV检测的对照。ISH方法使用针对EBV“W”重复区域的探针,用人胎盘DNA探针作为样本制备的对照。PCR方法扩增长内部直接重复序列中的一个110碱基对区域,并以β-肌动蛋白的扩增作为DNA保存的对照。两种检测均使用福尔马林固定石蜡包埋的Raji细胞作为阳性对照。

结果

8例IPSID患者中,ISH和PCR均未检测到EBV:7个DNA保存良好的对照样本中,1个样本用PCR检测结果为阳性,但用ISH检测为阴性。

结论

这些发现不支持EBV在IPSID中诱导B细胞增殖中起作用。

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