Acosta-Ampudia Yeny, Monsalve Diana M, Castillo-Medina Luis F, Rodríguez Yhojan, Pacheco Yovana, Halstead Susan, Willison Hugh J, Anaya Juan-Manuel, Ramírez-Santana Carolina
Center for Autoimmune Diseases Research, School of Medicine and Health Sciences, Universidad del Rosario, Bogota, Colombia.
Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.
Front Mol Neurosci. 2018 Apr 11;11:116. doi: 10.3389/fnmol.2018.00116. eCollection 2018.
Zika virus (ZIKV) is an emerging flavivirus rapidly spreading throughout the tropical Americas. mosquitoes is the principal way of transmission of the virus to humans. ZIKV can be spread by transplacental, perinatal, and body fluids. ZIKV infection is often asymptomatic and those with symptoms present minor illness after 3 to 12 days of incubation, characterized by a mild and self-limiting disease with low-grade fever, conjunctivitis, widespread pruritic maculopapular rash, arthralgia and myalgia. ZIKV has been linked to a number of central and peripheral nervous system injuries such as Guillain-Barré syndrome (GBS), transverse myelitis (TM), meningoencephalitis, ophthalmological manifestations, and other neurological complications. Nevertheless, mechanisms of host-pathogen neuro-immune interactions remain incompletely elucidated. This review provides a critical discussion about the possible mechanisms underlying the development of autoimmune neurological conditions associated with Zika virus infection.
寨卡病毒(ZIKV)是一种新出现的黄病毒,正在迅速蔓延至整个热带美洲地区。蚊子是该病毒传播给人类的主要途径。寨卡病毒可通过胎盘、围产期及体液传播。寨卡病毒感染通常无症状,有症状者在潜伏期3至12天后出现轻微病症,其特征为一种轻度自限性疾病,伴有低热、结膜炎、广泛瘙痒性斑丘疹、关节痛和肌痛。寨卡病毒与多种中枢和外周神经系统损伤有关,如吉兰-巴雷综合征(GBS)、横贯性脊髓炎(TM)、脑膜脑炎、眼科表现及其他神经并发症。然而,宿主-病原体神经免疫相互作用的机制仍未完全阐明。本综述对与寨卡病毒感染相关的自身免疫性神经疾病发生的潜在机制进行了批判性讨论。