Open AccessThe clinical spectrum and immunopathological mechanisms underlying ZIKV-induced neurological manifestations
Author(s) -
Igor Salerno Filgueiras,
Amanda Torrentes de Carvalho,
Daniela P. Cunha,
Dennyson Leandro M. Fonseca,
Nadia El Khawanky,
Paula Paccielli Freire,
Gustavo Cabral-Miranda,
Lena Friederike Schimke,
Niels Olsen Saraiva Câmara,
Hans D. Ochs,
Jean Pierre Schatzmann Peron,
Otávio Cabral-Marques,
Zilton Farias Meira de Vasconcelos
Publication year - 2021
Publication title -
plos neglected tropical diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.99
H-Index - 135
eISSN - 1935-2735
pISSN - 1935-2727
DOI - 10.1371/journal.pntd.0009575
Subject(s) - zika virus , microcephaly , medicine , immunology , neuropathology , virology , disease , virus , pathology , pediatrics
Since the 2015 to 2016 outbreak in America, Zika virus (ZIKV) infected almost 900,000 patients. This international public health emergency was mainly associated with a significant increase in the number of newborns with congenital microcephaly and abnormal neurologic development, known as congenital Zika syndrome (CZS). Furthermore, Guillain–Barré syndrome (GBS), a neuroimmune disorder of adults, has also been associated with ZIKV infection. Currently, the number of ZIKV-infected patients has decreased, and most of the cases recently reported present as a mild and self-limiting febrile illness. However, based on its natural history of a typical example of reemerging pathogen and the lack of specific therapeutic options against ZIKV infection, new outbreaks can occur worldwide, demanding the attention of researchers and government authorities. Here, we discuss the clinical spectrum and immunopathological mechanisms underlying ZIKV-induced neurological manifestations. Several studies have confirmed the tropism of ZIKV for neural progenitor stem cells by demonstrating the presence of ZIKV in the central nervous system (CNS) during fetal development, eliciting a deleterious inflammatory response that compromises neurogenesis and brain formation. Of note, while the neuropathology of CZS can be due to a direct viral neuropathic effect, adults may develop neuroimmune manifestations such as GBS due to poorly understood mechanisms. Antiganglioside autoantibodies have been detected in multiple patients with ZIKV infection–associated GBS, suggesting a molecular mimicry. However, further additional immunopathological mechanisms remain to be uncovered, paving the way for new therapeutic strategies.