Prevalence of IgG Autoantibodies against GD3 Ganglioside in Acute Zika Virus Infection.
Prevalence of IgG Autoantibodies against GD3 Ganglioside in Acute Zika Virus Infection.
复制标题
DOI：
10.3389/fmed.2018.00025
复制
发表时间：
2018
影响因子：
3.9
通讯作者：
Morrot A
中科院分区：
文献类型：
--
作者：
Nico D;Conde L;Rivera-Correa JL;Vasconcelos-Dos-Santos A;Mesentier-Louro L;Freire-de-Lima L;Arruda MB;Freire-de-Lima CG;Ferreira ODC Jr;Lopes Moreira ME;Zin AA;Vasconcelos ZFM;Otero RM;Palatnik-de-Sousa CB;Tanuri A;Todeschini AR;Savino W;Rodriguez A;Morrot A
寨卡病毒(Zika Virus，ZIKV)病已成为全球卫生突发事件，对公众健康造成毁灭性影响。最近的证据表明，该病毒是一种紧急神经病原体，促进了人类神经系统的严重病理，包括破坏性和畸形后果，如眼睛和胎儿脑损伤的发展，新生儿小头畸形，以及成人的格林-巴利综合征(GBS)。这些中枢和外周神经系统的神经系统疾病被认为与病毒的嗜神经性有关，这种病毒具有感染神经干细胞和外周神经元的能力，这是其致病性的标志。抗神经节苷脂自身抗体的存在在GBS和多种神经系统疾病的发病机制中起着关键作用。神经节苷脂是一类含半乳糖的脑苷脂，主要在神经系统组织中表达，在神经细胞的生理和神经发生中起着重要作用。因此，我们的研究结果表明，在没有任何神经系统症状的ZIKV感染急性期患者，抗GD3神经节苷脂的抗体水平升高。GD3神经节苷脂是一种在神经干细胞中高表达的糖脂，在维持其自我更新细胞能力方面发挥作用。这些抗体的病理阈值可能只在继发或随后的感染中获得。根据这些证据，我们认为自身免疫反应的靶点GD3可能在ZIKV感染时出现的神经病变和神经发生障碍中起作用。
Zika virus (ZIKV) disease has become a global health emergency with devastating effects on public health. Recent evidences implicate the virus as an emergent neuropathological agent promoting serious pathologies of the human nervous system, that include destructive and malformation consequences such as development of ocular and fetal brain lesions, microcephaly in neonates, and Guillain–Barré syndrome (GBS) in adults. These neurological disorders of both central and peripheral nervous systems are thought to be associated to the neurotropic properties of the virus that has ability to infect neural stem cells as well as peripheral neurons, a hallmark of its pathogenicity. The presence of autoantibodies against gangliosides plays a pivotal role in the etiogenesis of GBS and a variety of neurological disorders. Gangliosides are a class of galactose-containing cerebrosides mainly expressed in nervous system tissues playing a critical role in the physiology of neural cells and neurogenesis. Herein, our findings indicate that patients at acute phase of ZIKV infection without any neurological signs show increased levels of IgG autoantibody against GD3 gangliosides, a class of glycolipid found to be highly expressed in neural stem cell acting in the maintenance of their self-renewal cellular capacity. It is possible that a pathological threshold of these antibodies is only acquired in secondary or subsequent infections. In the light of these evidences, we propose that the target of GD3 by autoimmune responses may possibly has an effect in the neuropathy and neurogenesis disorder seen during ZIKV infection.