Widespread dietary exposure of the population of Britain to bovine spongiform encephalopathy (BSE) prions in the 1980s and 1990s led to the emergence of variant Creutzfeldt-Jakob Disease (vCJD) in humans. Two previous appendectomy sample surveys (Appendix-1 and -2) estimated the prevalence of abnormal prion protein (PrP) in the British population exposed to BSE to be 237 per million and 493 per million, respectively. The Appendix-3 survey was recommended to measure the prevalence of abnormal PrP in population groups thought to have been unexposed to BSE. Immunohistochemistry for abnormal PrP was performed on 29,516 samples from appendices removed between 1962 and 1979 from persons born between 1891 through 1965, and from those born after 1996 that had been operated on from 2000 through 2014. Seven appendices were positive for abnormal PrP, of which two were from the pre-BSE-exposure era and five from the post BSE-exposure period. None of the seven positive samples were from appendices removed before 1977, or in patients born after 2000 and none came from individuals diagnosed with vCJD. There was no statistical difference in the prevalence of abnormal PrP across birth and exposure cohorts. Two interpretations are possible. Either there is a low background prevalence of abnormal PrP in human lymphoid tissues that may not progress to vCJD. Alternatively, all positive specimens are attributable to BSE exposure, a finding that would necessitate human exposure having begun in the late 1970s and continuing through the late 1990s.

中文翻译：

---

英国在接触牛疯牛病流行前后人类阑尾中异常朊病毒蛋白的流行情况。


20 世纪 80 年代和 90 年代，英国民众普遍通过饮食接触牛海绵状脑病 (BSE) 朊病毒，导致人类出现变异型克雅氏病 (vCJD)。之前的两次阑尾切除术抽样调查（附录-1和-2）估计，在暴露于BSE的英国人群中，异常朊病毒蛋白（PrP）的患病率分别为每百万人237人和每百万人493人。建议采用附录 3 调查来测量被认为未接触过 BSE 的人群中异常 PrP 的患病率。对 1962 年至 1979 年间摘除的 29,516 个阑尾样本进行了异常 PrP 的免疫组织化学检查，这些样本来自 1891 年至 1965 年出生的人，以及 1996 年以后出生且在 2000 年至 2014 年期间接受过手术的人。 7 个阑尾呈异常 PrP 阳性，其中两个来自 BSE 暴露前时期，五个来自 BSE 暴露后时期。这七个阳性样本中没有一个来自 1977 年之前切除的阑尾，也不是 2000 年之后出生的患者，也没有一个来自诊断为 vCJD 的个体。出生组和暴露组中异常 PrP 的患病率没有统计学差异。有两种解释是可能的。要么人类淋巴组织中异常 PrP 的背景患病率较低，可能不会发展为 vCJD。或者，所有阳性样本都可归因于 BSE 暴露，这一发现使得人类暴露必须从 20 世纪 70 年代末开始，一直持续到 90 年代末。