Characterization of Urucuri Virus (BeAn 100049), a new member of the Bunyaviridaie group. Ultrastructural study of experimentally infected mouse brain

Trabalho executado no Núcleo de Patologia Regional e Higiene da Universidade Federal do Pará e Instituto Evandro Chagas da Fundação Serviço Especial de Saúde Pública. Integrante de pesquisa conjunta com o Instituto de Medicina Tropical de Hamburgo. Alemanha. segundo convênio CNPq-KFA. Projeto SIP/02- 006 do Programa dos Trópicos Úmidos do CNPqUniversidade Federal do Pará. Núcleo de Patologia Regional e Higiene. Seção de Microscopia Eletrônica. Belém, PA, Brasil.Universidade Federal do Pará. Núcleo de Patologia Regional e Higiene. Laboratório de Microscopia Eletrônica. Belém, PA, Brasil.Ministério da Saúde. Fundação Serviços de Saúde Pública. Instituto Evandro Chagas. Belém, PA, Brasil.Universidade Federal do Pará. Núcleo de Patologia Regional e Higiene. Laboratório de Experimentação Animal. Belém, PA, Brasil.Instituto de Medicina Tropical. Secção de Virologia. Hamburgo.A inoculação experimental de camundongos albinos recém-nascidos por via intra-cerebral com o vírus Urucuri para estudos da patologia virótica permitiu a documentação, pela primeira vez, da partícula deste agente e seu locus de multiplicação. O vírlon tem contorno circular ou levemente elíptico, medindo em média 105 nm, com cerne de eletrondensidade variável e envelope com projeções mui pequenas ou inaparentes. As partículas são formadas nas vesículas do complexo de Golgi e parecem ser eliminadas da célula por processo de exocitose, sem necessidade de ruptura da membrana plasmática ou necrose celular. Estas caracteristicas permitem a classificação do virus no grupo taxonômico dos Bunyaviridae. Não foram detectados os locais de acúmulo das partículas.Thin section electron microscopic examination of white mice brain experimentally inoculated wIth Urucuri Virus (BeAn 100049) resulted in the documentation of morphology and morphogenesls of the vírus particles. Most particles are round, some are lightly oval, with a mean diamerer of approximately 100 nm (variation between 75 and 122 nm), with a core of variable electrondensity and a membranelike envelope with a surface projetion layer. Virus particles are formed within cisternae of the Golgi complex of neurons where they accumulate in small groups or individually. It is suggested that vIrus is released from infected neurons by vesicular membrane fusion and exocytosis. These flndings prove that the Urucuri virus belongs to the Bunyaviridae taxonomic group or "family

In situ immune response and mechanisms of cell damage in central nervous system of fatal cases microcephaly by Zika virus

Abstract Zika virus (ZIKV) has recently caused a pandemic disease, and many cases of ZIKV infection in pregnant women resulted in abortion, stillbirth, deaths and congenital defects including microcephaly, which now has been proposed as ZIKV congenital syndrome. This study aimed to investigate the in situ immune response profile and mechanisms of neuronal cell damage in fatal Zika microcephaly cases. Brain tissue samples were collected from 15 cases, including 10 microcephalic ZIKV-positive neonates with fatal outcome and five neonatal control flavivirus-negative neonates that died due to other causes, but with preserved central nervous system (CNS) architecture. In microcephaly cases, the histopathological features of the tissue samples were characterized in three CNS areas (meninges, perivascular space, and parenchyma). The changes found were mainly calcification, necrosis, neuronophagy, gliosis, microglial nodules, and inflammatory infiltration of mononuclear cells. The in situ immune response against ZIKV in the CNS of newborns is complex. Despite the predominant expression of Th2 cytokines, other cytokines such as Th1, Th17, Treg, Th9, and Th22 are involved to a lesser extent, but are still likely to participate in the immunopathogenic mechanisms of neural disease in fatal cases of microcephaly caused by ZIKV

Zika Virus Epidemic in Brazil. II. Post-Mortem Analyses of Neonates with Microcephaly, Stillbirths, and Miscarriage

Introduction: The recent Zika virus(ZIKV) epidemic in Brazil was characterized by a range of different clinical presentations, particularly microcephaly, Guillain-Barré syndrome, and death. In this context, we determined the causal relationship between fatal microcephaly cases and ZIKV infection. Methods: Twelve fatal cases of neonates, whose mothers were infected with ZIKV during pregnancy, were examined; cases included nine neonatal deaths due to microcephaly, one miscarriage, and two stillbirths. Tissue samples were obtained from all cases at necropsy and were submitted for virological investigation (RT-qPCR and virus isolation) and/or histopathology (hematoxylin and eosin staining) and immunohistochemical assay for the detection of ZIKV antigens. Results: ZIKV antigens and/or ZIKV RNA were detected in tissue samples of all 12 cases examined. ZIKV was recovered in one case. Results of the virological and immunohistochemical analyses, as well as the anatomic abnormalities and histopathologic changes observed at necropsy on the 12 fatal cases, are presented. Conclusions: Data from these 12 cases provide strong evidence of the causal relationship between ZIKV and congenital disease in fetuses of women who were infected with the virus during pregnancy