Antibodies to JC and BK viruses among persons with non-Hodgkin lymphoma
Antibodies to JC and BK viruses among persons with non-Hodgkin lymphoma
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DOI：
10.1002/ijc.21277
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发表时间：
2005-12-20
影响因子：
6.4
通讯作者：
Viscidi, RP
中科院分区：
文献类型：
--
作者：
Engels, EA;Rollison, DE;Viscidi, RP
y两种相关的多核病毒，JC 病毒 (JCV) 和 BK 病毒 (BKV)，通常会导致人类终身感染，并定期重新激活，表现为尿液中病毒脱落。由于 JCV 可以感染淋巴细胞并引起染色体损伤，因此它可能会引起非霍奇金淋巴瘤 (NHL)。为了检验这一假设，我们使用病毒样颗粒酶免疫测定法在 3 组不同的受试者中测量了针对 JCV 和 BKV 衣壳的 IgG 抗体。首先，在美国一项基于人群的 NHL 病例对照研究（724 例病例，622 例对照）中，我们发现病例中的 JCV 抗体水平低于对照（中位光密度 = 0.12 与 0.21，p < 0.0001）；同样，JCV 血清阳性率在病例中较低（49% vs. 59%，调整后优势比 [OR] = 0.70，95% 置信区间 [CI] = 0.56-0.87）。相比之下，BKV 抗体水平在各组之间没有差异。其次，我们发现 24 名接受化疗的 NHL 患者的 JCV 和 BKV 抗体水平随时间变化不大。第三，我们评估了 126 名同性恋男性，其中 46 名通过尿液排出 JCV，14 名通过尿液排出 BKV。脱落者的抗体水平比非脱落者高得多（JCV：中位光密度= 0.67 vs. 0.07，p < 0.0001；BKV：0.87 vs. 0.40，p = 0.003），表明这些抗体是病毒复制的标记。由于在 NHL 病例中未发现 BKV 抗体缺乏，并且化疗后抗体水平没有发生重大变化，因此我们认为在 NHL 患者中观察到的 JCV 抗体水平较低可能并不完全是由于疾病或治疗效果所致。需要进行更多研究来确定 NHL 个体中 JCV 复制是否减少，以及这些发现是否与 JCV 在 NHL 中的病因作用一致。 (c) 2005 年 Wiley-Liss, Inc.
yTwo related polyornaviruses, JC virus (JCV) and BK virus (BKV), commonly cause lifelong infections in humans, with periodic reactivation manifesting as viral shedding in urine. Because JCV can infect lymphocytes and cause chromosomal damage, it is a plausible candidate to cause non-Hodgkin lymphoma (NHL). To test this hypothesis, we measured IgG antibodies to JCV and BKV capsids using a virus-like particle enzyme immunoassay in 3 separate groups of subjects. First, in a U.S. population-based case-control study of NHL (724 cases, 622 controls), we found lower JCV antibody levels in cases than controls (median optical density = 0.12 vs. 0.21, p < 0.0001); likewise, JCV seroprevalence was lower in cases (49% vs. 59%, adjusted odds ratio [OR] = 0.70, 95% confidence interval [CI] = 0.56-0.87). In contrast, BKV antibody levels did not differ between groups. Second, we found that JCV and BKV antibody levels changed little over time among 24 NHL patients receiving chemotherapy. Third, we evaluated 126 homosexual men, of whom 46 were shedding JCV and 14 were shedding BKV in urine. Antibody levels were much higher in shedders than non-shedders (JCV: median optical density = 0.67 vs. 0.07, p < 0.0001; BKV: 0.87 vs. 0.40, p = 0.003), indicating that these antibodies are a marker for viral replication. Because no deficit of BKV antibody was seen in NHL cases, and because antibody levels did not change materially with chemotherapy, we suggest that the lower levels of JCV antibody observed in NHL patients may not be due entirely to a disease or treatment effect. Additional research is needed to determine whether JCV replication is decreased in individuals with NHL and whether these findings are consistent with an etiologic role for JCV in NHL. (c) 2005 Wiley-Liss, Inc.