The clinical spectrum and immunopathological mechanisms underlying ZIKV-induced neurological manifestations

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Filgueiras, Igor Salerno ^[1] ; Torrentes de Carvalho, Amanda ^[2] ; Cunha, Daniela Prado ^[3] ; Mathias da Fonseca, Dennyson Leandro ^[4] ; El Khawanky, Nadia ^[5] ; Freire, Paula Paccielli ^[1] ; Cabral-Miranda, Gustavo ; Schimke, Lena F. ; Camara, Niels Olsen Saraiva ^[1] ; Ochs, Hans D. ^{[6, 7]} ; Peron, Jean Pierre Schatzmann ^[1] ; Cabral-Marques, Otavio ^{[4, 1, 8]} ; de Vasconcelos, Zilton Farias Meira ^[3]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Dept Immunol, Inst Biomed Sci, Sao Paulo - Brazil

^[2] Fed Univ Fluminense, Dept Immunobiol, Inst Biol, Rio De Janeiro - Brazil

^[3] Fiocruz MS, Inst Fernandes Figueira, Dept Clin Res, Rio De Janeiro - Brazil

^[4] Univ Sao Paulo, Sch Pharmaceut Sci, Dept Clin Anal & Toxicol, Sao Paulo - Brazil

^[5] Univ Freiburg, Dept Hematol & Oncol, Fac Med, Freiburg - Germany

^[6] Univ Washington, Sch Med, Dept Pediat, Seattle, WA 98195 - USA

^[7] Seattle Childrens Res Inst, Seattle, WA - USA

^[8] Univ Sci Educ & Res Network USERN, Network Immun Infect Malignancy & Autoimmun NIIMA, Sao Paulo - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: PLoS Neglected Tropical Diseases; v. 15, n. 8 AUG 2021.
• Citações Web of Science: 0

Resumo

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-Barre 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. (AU)

• Processo FAPESP: 18/18886-9 - Análise sistêmica e integrativa da resposta imune às infecções virais por Zika e Dengue
• Beneficiário: Otávio Cabral Marques
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores
• Processo FAPESP: 20/09146-1 - Análise sistêmica e integrativa dos mecanismos moleculares associados à imunorregulação em pacientes com COVID-19
• Beneficiário: Paula Paccielli Freire-Barguil
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 17/05264-7 - Metabolismo celular, microbiota e sistema imune: novos paradigmas na fisiopatologia das doenças renais
• Beneficiário: Niels Olsen Saraiva Câmara
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 20/01688-0 - Análise sistêmica e integrativa da resposta imune às infecções virais por Zika e Dengue
• Beneficiário: Otávio Cabral Marques
• Modalidade de apoio: Bolsas no Brasil - Jovens Pesquisadores