Herpes simplex virus type 1 has the ability to induce expression of a human gene cluster located on chromosome 19 upon infection. This gene cluster contains three fucosyltransferases (encoded by FUT3, FUT5 and FUT6) with the ability to add a fucose to an N-acetylglucosamine residue. Little is known regarding the transcriptional activation of these three genes in human cells. Intriguingly, herpes simplex virus type 1 activates all three genes simultaneously during infection, a situation not observed in uninfected tissue, pointing towards a virus specific mechanism for transcriptional activation. The aim of this study was to define the underlying mechanism for the herpes simplex virus type 1 activation of FUT3, FUT5 and FUT6 transcription. The transcriptional activation of the FUT gene cluster on chromosome 19 in fibroblasts was specific, not involving adjacent genes. Moreover, inhibition of NFκB signaling through panepoxydone treatment significantly decreased the induction of FUT3, FUT5 and FUT6 transcriptional activation, as did siRNA targeting of p65 in herpes simplex virus type 1 infected fibroblasts. NFκB and p65 signaling appears to play an important role in the regulation of FUT3, FUT5 and FUT6 transcriptional activation by herpes simplex virus type 1 although additional, unidentified, viral factors might account for part of the mechanism as direct interferon mediated stimulation of NFκB was not sufficient to induce the fucosyltransferase encoding gene cluster in uninfected cells.

中文翻译：

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1型单纯疱疹病毒的NFκB介导的细胞FUT3、5和6基因簇的激活

1型单纯疱疹病毒在感染后具有诱导位于19号染色体上的人类基因簇表达的能力。该基因簇包含三个岩藻糖基转移酶（由FUT3，FUT5和FUT6编码），具有将岩藻糖添加到N-乙酰氨基葡萄糖残基的能力。关于这三种基因在人类细胞中的转录激活知之甚少。有趣的是，1型单纯疱疹病毒在感染过程中同时激活了所有三个基因，这种情况在未感染的组织中未发现，这表明病毒具有转录激活的特定机制。这项研究的目的是确定单纯疱疹病毒1型激活FUT3，FUT5的潜在机制。和FUT6转录。FUT基因簇在成纤维细胞19号染色体上的转录激活是特异性的，不涉及相邻基因。此外，通过帕潘西酮治疗抑制NFκB信号显着降低了FUT3，FUT5和FUT6转录激活的诱导，就像在单纯疱疹病毒1型感染的成纤维细胞中靶向p65的siRNA一样。NFκB和p65信号似乎在FUT3，FUT5和FUT6的调节中起重要作用 1型单纯疱疹病毒的转录激活，尽管其他的，未知的病毒因素可能是部分机制，因为直接干扰素介导的NFκB刺激不足以诱导未感染细胞中岩藻糖基转移酶编码基因簇。