NF kappa B-mediated activation of the cellular FUT3, 5 and 6 gene cluster by herpes simplex virus type 1

作者：Norden Rickard^*; Samuelsson Ebba; Nystrom Kristina

来源：Glycobiology, 2017, 27(11): 999-1005.

DOI：10.1093/glycob/cwx079

• FUT3
• FUT5
• FUT6
• Herpes simplex virus type 1
• NF kappa B

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 NF kappa B 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. NF kappa B 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 NF kappa B was not sufficient to induce the fucosyltransferase encoding gene cluster in uninfected cells.

• 出版日期2017-11