Zhu Liqian, Thunuguntla Prasanth, Liu Yilin, Hancock Morgan, Jones Clinton
Oklahoma State University Center for Veterinary Health Sciences Department of Veterinary Pathobiology Stillwater, OK 74078, USA; Yangzhou University, College of Veterinary Medicine and Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonosis, 48 Wenhui East Road, Yangzhou 225009, China.
Oklahoma State University Center for Veterinary Health Sciences Department of Veterinary Pathobiology Stillwater, OK 74078, USA.
Virology. 2017 Jan;500:91-95. doi: 10.1016/j.virol.2016.10.014. Epub 2016 Oct 24.
Bovine herpes virus 1 (BoHV-1), an important bovine pathogen, causes conjunctivitis and disorders in the upper respiratory tract. Following acute infection, BoHV1 establishes life-long latency in sensory neurons. Recent studies demonstrated that viral gene products expressed in trigeminal ganglionic neurons during latency stabilize β-catenin levels, an important signaling molecule that interacts with a family of DNA binding proteins (T-cell factors) and subsequently stimulates transcription. In this study, we provide new evidence demonstrating that BoHV-1 transiently increased β-catenin protein levels in bovine kidney (CRIB) cells, but not in rabbit skin cells. β-catenin dependent transcription was also stimulated by infection of CRIB cells. The β-catenin small molecule inhibitor (iCRT14) significantly reduced the levels of BoHV-1 virus during productive infection of CRIB cells and rabbit skin cells. In summary, these studies suggested the ability of β-catenin to stimulate cell survival and cell cycle regulatory factors enhances productive infection in non-neuronal cells.
牛疱疹病毒1型（BoHV-1）是一种重要的牛病原体，可引起结膜炎和上呼吸道疾病。急性感染后，BoHV-1在感觉神经元中建立终身潜伏感染。最近的研究表明，潜伏期三叉神经节神经元中表达的病毒基因产物可稳定β-连环蛋白水平，β-连环蛋白是一种重要的信号分子，可与一类DNA结合蛋白（T细胞因子）相互作用并随后刺激转录。在本研究中，我们提供了新的证据表明，BoHV-1可短暂增加牛肾（CRIB）细胞中β-连环蛋白的蛋白水平，但在兔皮肤细胞中则不然。CRIB细胞感染后也会刺激β-连环蛋白依赖性转录。β-连环蛋白小分子抑制剂（iCRT14）在CRIB细胞和兔皮肤细胞的生产性感染期间显著降低了BoHV-1病毒的水平。总之，这些研究表明，β-连环蛋白刺激细胞存活和细胞周期调节因子的能力增强了非神经元细胞中的生产性感染。
