Zika virus congenital syndrome: experimental models and clinical aspects

Autor(es)

Polonio, Carolina Manganeli ^[1] ; de Freitas, Carla Longo ^[1] ; Zanluqui, Nagela Ghabdan ^[1] ; Peron, Jean Pierre Schatzmann ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Neuroimmune Interact Lab, Dept Immunol, ICB 4, Ave Prof Lineu Prestes, 1730, Cidade Univ, BR-05508900 Sao Paulo, SP - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: Journal of Venomous Animals and Toxins including Tropical Diseases; v. 23, SEP 15 2017.
• Citações Web of Science: 4

Resumo

Viral infections have long been the cause of severe diseases to humans, increasing morbidity and mortality rates worldwide, either in rich or poor countries. Yellow fever virus, H1N1 virus, HIV, dengue virus, hepatitis B and C are well known threats to human health, being responsible for many million deaths annually, associated to a huge economic and social cost. In this context, a recently introduced flavivirus in South America, called Zika virus (ZIKV), led the WHO to declare in February 1st 2016 a warning on Public Health Emergency of International Concern (PHEIC). ZIKV is an arbovirus of the Flaviviridae family firstly isolated from sentinels Rhesus sp. monkeys at the Ziika forest in Uganda, Africa, in 1947. Lately, the virus has well adapted to the worldwide spread Aedes aegypti mosquito, the vector for DENV, CHIKV, YFV and many others. At first, it was not considered a threat to human health, but everything changed when a skyrocketing number of babies born with microcephaly and adults with Guillain-Barre syndrome were reported, mainly in northeastern Brazil. It is now well established that the virus is responsible for the so called congenital Zika syndrome (CZS), whose most dramatic features are microcephaly, arthrogryposis and ocular damage. Thus, in this review, we provide a brief discussion of these main clinical aspects of the CZS, correlating them with the experimental animal models described so far. (AU)

• Processo FAPESP: 11/18703-2 - O papel do eixo triptofano - Kinureninas na regulação da resposta imune através de receptores de glutamato tipo NMDA na encefalomielite experimental auto-imune e na lesão por isquemia e reperfusão cerebral
• Beneficiário: Jean Pierre Schatzmann Peron
• Linha de fomento: Auxílio à Pesquisa - Apoio a Jovens Pesquisadores