没有证据表明 Merkel 细胞多瘤病毒在角化棘皮瘤中起因果作用。
No evidence for a causal role of Merkel cell polyomavirus in keratoacanthoma.
机构信息
Institute of Virology, National Reference Centre for Papilloma- and Polyomaviruses, University of Cologne, Cologne, Germany.
出版信息
J Am Acad Dermatol. 2012 Jul;67(1):41-6. doi: 10.1016/j.jaad.2011.07.026. Epub 2011 Oct 11.
BACKGROUND
Merkel cell polyomavirus (MCPyV) is a recently discovered virus that is monoclonally integrated into the genome of approximately 80% of all Merkel cell carcinomas (MCCs). While some evidence exists that MCPyV does not play a pathogenic role in other nonmelanoma skin cancers, such as basal cell carcinoma and squamous cell carcinoma (SCC), little is known about the presence of MCPyV in keratoacanthoma (KA).
OBJECTIVES
To evaluate the prevalence, viral DNA-load, and large T(umor)-antigen expression of MCPyV in KA of immunocompetent patients and to compare the results with those found in SCC and MCC.
METHODS
Paraffin-embedded tissue samples were analyzed for the presence of MCPyV-DNA by polymerase chain reaction (PCR). MCPyV-DNA load (MCPyV-DNA copies per beta-globin gene copy) was determined by using quantitative real-time PCR. Immunohistochemical analysis of the MCPyV large T-antigen was performed with the monoclonal antibody CM2B4.
RESULTS
A total of 137 samples (42 KA, 52 SCC, and 43 MCC) were analyzed. MCPyV-DNA was found significantly more frequently in MCC (37/43, 86.0%) compared with KA (12/42, 28.6%) and SCC (14/52, 26.9%). Moreover, MCPyV-DNA loads were more than two orders of magnitude lower in KA and SCC compared with MCC (median/mean loads 0.005/0.015 [KA] vs 0.023/0.059 [SCC] vs 2.613/56.840 [MCC] MCPyV-DNA copies per beta-globin gene copy). All MCC analyzed (n = 3) expressed MCPyV large T-antigen, whereas 8 KA and 7 SCC were negative in immunohistochemistry.
LIMITATIONS
The relatively small number of samples is a limitation.
CONCLUSIONS
Our findings argue against a pathogenic role of MCPyV in KA and SCC.
背景
Merkel 细胞多瘤病毒（MCPyV）是一种最近发现的病毒，大约 80%的 Merkel 细胞癌（MCC）中都存在单克隆整合到基因组中的 MCPyV。虽然有证据表明 MCPyV 在其他非黑色素瘤皮肤癌（如基底细胞癌和鳞状细胞癌[SCC]）中不具有致病性作用，但关于 MCPyV 在角化棘皮瘤（KA）中的存在知之甚少。
目的
评估免疫功能正常的患者中 KA 中 MCPyV 的流行率、病毒 DNA 载量和大 T（umor）-抗原表达，并将结果与 SCC 和 MCC 进行比较。
方法
通过聚合酶链反应（PCR）分析石蜡包埋组织样本中 MCPyV-DNA 的存在。通过实时定量 PCR 确定 MCPyV-DNA 载量（MCPyV-DNA 拷贝数/β-球蛋白基因拷贝数）。使用单克隆抗体 CM2B4 进行 MCPyV 大 T 抗原的免疫组织化学分析。
结果
共分析了 137 个样本（42 个 KA、52 个 SCC 和 43 个 MCC）。与 KA（12/42，28.6%）和 SCC（14/52，26.9%）相比，MCC（37/43，86.0%）中 MCPyV-DNA 的检出频率显著更高。此外，与 MCC 相比，KA 和 SCC 中的 MCPyV-DNA 载量低两个数量级以上（中位数/平均值负载 0.005/0.015[KA]vs 0.023/0.059[SCC]vs 2.613/56.840 [MCC]MCPyV-DNA 拷贝数/β-球蛋白基因拷贝数）。分析的所有 MCC（n=3）均表达 MCPyV 大 T 抗原，而 8 个 KA 和 7 个 SCC 在免疫组织化学中为阴性。
局限性
样本数量相对较少是一个限制。
结论
我们的研究结果表明，MCPyV 在 KA 和 SCC 中不具有致病性作用。
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