Wang Wei, Wang Xin, Yang Lianwei, Fu Wenkun, Pan Dequan, Liu Jian, Ye Jianghui, Zhao Qinjian, Zhu Hua, Cheng Tong, Xia Ningshao
State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, National Institute of Diagnostics and Vaccine Development in Infectious Diseases, School of Life Science, Xiamen University, Xiamen 361102, PR China.
Department of Microbiology and Molecular Genetics, New Jersey Medical School, Rutgers University, 225 Warren Street, Newark, NJ 070101, USA.
Virology. 2016 Apr;491:96-105. doi: 10.1016/j.virol.2016.01.019. Epub 2016 Feb 15.
Varicella-zoster virus (VZV) is the causative agent of both chickenpox (varicella) and shingles (zoster). VZV survives host defenses, even with an intact immune system, and disseminates in the host before causing disease. To date, several diverse immunomodulatory strategies used by VZV to undermine host immunity have been identified; however, few studies have addressed the complement evasion strategies used by this virus. Here, we show that expression of CD59, which is a key member of host regulators of complement activation (RCA), is significantly upregulated in response to VZV infection in human T cells and dorsal root ganglia (DRG) but not in human skin xenografts in SCID-hu mice in vivo. This is the first report demonstrating that VZV infection upregulates host CD59 expression in a tissue-specific manner in vivo, which may aid VZV in complement evasion and pathogenesis.
水痘带状疱疹病毒（VZV）是水痘（水痘）和带状疱疹（带状疱疹）的病原体。即使免疫系统完好，VZV仍能抵御宿主防御，并在引发疾病之前在宿主体内传播。迄今为止，已经确定了VZV用于破坏宿主免疫的几种不同免疫调节策略；然而，很少有研究涉及该病毒使用的补体逃避策略。在这里，我们表明，作为补体激活宿主调节因子（RCA）的关键成员，CD59的表达在人T细胞和背根神经节（DRG）中对VZV感染有显著上调，但在体内SCID-hu小鼠的人皮肤异种移植中则没有。这是第一份证明VZV感染在体内以组织特异性方式上调宿主CD59表达的报告，这可能有助于VZV逃避补体和发病机制。
