Gan Lu, O'Hanlon Terrance P, Lai Zhennan, Fannin Rick, Weller Melodie L, Rider Lisa G, Chiorini John A, Miller Frederick W
Environmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, Maryland, United States of America.
Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, United States of America.
PLoS One. 2015 Nov 10;10(11):e0142486. doi: 10.1371/journal.pone.0142486. eCollection 2015.
Viral agents are of interest as possible autoimmune triggers due to prior reported associations and widely studied molecular mechanisms of antiviral immune responses in autoimmunity. Here we examined new viral candidates for the initiation and/or promotion of systemic autoimmune diseases (SAID), as well as possible related signaling pathways shared in the pathogenesis of those disorders. RNA isolated from peripheral blood samples from 33 twins discordant for SAID and 33 matched, unrelated healthy controls was analyzed using a custom viral-human gene microarray. Paired comparisons were made among three study groups-probands with SAID, their unaffected twins, and matched, unrelated healthy controls-using statistical and molecular pathway analyses. Probands and unaffected twins differed significantly in the expression of 537 human genes, and 107 of those were associated with viral infections. These 537 differentially expressed human genes participate in overlapping networks of several canonical, biologic pathways relating to antiviral responses and inflammation. Moreover, certain viral genes were expressed at higher levels in probands compared to either unaffected twins or unrelated, healthy controls. Interestingly, viral gene expression levels in unaffected twins appeared intermediate between those of probands and the matched, unrelated healthy controls. Of the viruses with overexpressed viral genes, herpes simplex virus-2 (HSV-2) was the only human viral pathogen identified using four distinct oligonucleotide probes corresponding to three HSV-2 genes associated with different stages of viral infection. Although the effects from immunosuppressive therapy on viral gene expression remain unclear, this exploratory study suggests a new approach to evaluate shared viral agents and antiviral immune responses that may be involved in the development of SAID.
由于先前报道的关联以及自身免疫中广泛研究的抗病毒免疫反应分子机制,病毒因子作为可能的自身免疫触发因素备受关注。在此,我们研究了引发和/或促进系统性自身免疫性疾病(SAID)的新病毒候选物,以及这些疾病发病机制中可能共享的相关信号通路。使用定制的病毒-人类基因微阵列分析了从33对患SAID的双胞胎及其33名匹配的、不相关的健康对照的外周血样本中分离的RNA。通过统计和分子通路分析,在三个研究组之间进行了配对比较,这三个研究组分别是患有SAID的先证者、其未受影响的双胞胎以及匹配的、不相关的健康对照。先证者和未受影响的双胞胎在537个人类基因的表达上存在显著差异,其中107个基因与病毒感染有关。这537个差异表达的人类基因参与了与抗病毒反应和炎症相关的几个经典生物学通路的重叠网络。此外,与未受影响的双胞胎或不相关的健康对照相比,某些病毒基因在先证者中的表达水平更高。有趣的是,未受影响的双胞胎中的病毒基因表达水平介于先证者和匹配的、不相关的健康对照之间。在病毒基因过表达的病毒中,单纯疱疹病毒2型(HSV-2)是唯一使用对应于与病毒感染不同阶段相关的三个HSV-2基因的四种不同寡核苷酸探针鉴定出的人类病毒病原体。尽管免疫抑制疗法对病毒基因表达的影响尚不清楚,但这项探索性研究提出了一种新方法,用于评估可能参与SAID发展的共享病毒因子和抗病毒免疫反应。