Search

The disease caused by each of the four serotypes of dengue virus (DENV) have plagued humans since last century. Symptoms of dengue virus (DENV) infection range from asymptomatic to dengue fever (DF) to severe dengue disease (SDD). One third of the world's population lives in regions with active urban DENV transmission, and thousands of serologically naive travelers visit these areas annually, making a significant portion of the human population at risk of being infected. Even though lifelong immunity to the homotypic serotype is achieved after a primary DENV infection. Heterotypic DENV infections may be exacerbated by a pre-existing immune memory to the primary infection and can result in an increased probability of severe disease. Not only, age, comorbidities and presence of antibodies transferred passively from dengue-immune mother to infants are considered risk factors to dengue severe forms. Plasma leakage and multiple organ impairment are well documented in the literature, affecting liver, lung, brain, muscle, and kidney. However, unusual manifestation, severe or not, have been reported and may require medical attention. This review will summarize and discuss the increasing reports of unusual manifestations in the clinical course of dengue infection.

Made available in DSpace on 2020-12-12T02:24:42Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-07-01 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) The association of Zika virus infection (ZIKV) with congenital malformation and neurological sequelae brought a significant global concern. Recent studies have shown that maternal viral infection leads to inflammation in the placental tissue. In this context, the antiinflammatory protein annexin 1 (ANXA1) has a major determination of the resolution of inflammation and it has been positively associated with antiparasitic activity in infected placental explants. Although these effects have been explored to some degree, ANXA1 expression and potential properties have not yet been fully elucidated in placentas infected with ZIKV. This study was conducted to evaluate the histopathology, inflammatory process and elucidate if ANXA1 were differently expressed in placentas of ZIKV-infected mothers. Three classification groups were used in this study: Neg/Neg (mother and placenta negative for the virus), Pos/Neg (infected mother, but no virus detected in placenta) and Pos/Pos (mother and placenta infected with ZIKV). ANXA1 was expressed in syncytiotrophoblast cells of all studied groups, and its expression was decreased in Pos/Neg group, which displayed also an increase of the inflammatory response, as evinced from the recruitment of inflammatory cells, increased levels of placenta cytokines, and evidence of impaired tissue repair. The presence of ZIKV in placentas of Pos/Pos group shows structural alterations, including detachment and disorganization of the trophoblastic epithelium. In summary, our results suggest that maternal infection with ZIKV, even without direct tissue infection, leads to a placental inflammatory response probably related to the modulation of ANXA1. After placental infection, structural changes - including inflammatory cells influx - are observed leading to placental dysfunction and reduced fetal weight. Our study sheds additional light on the outcomes of ZIKV infection in trophoblast and reveals a potential involvement of ANXA1 in the placental biology. Department of Biology School of Biosciences Humanities and Exact Sciences São Paulo State University (UNESP) Cell Biology Laboratory Institute of Health and Biological Sciences Federal University of Alagoas Department of Gynecology and Obstetrics São José Do Rio Preto School of Medicine (FAMERP) The William Harvey Research Institute Barts and the London School of Medicine Queen Mary University of London Department of Dermatological Infectious and Parasitic Diseases São José Do Rio Preto School of Medicine (FAMERP) Faceres School of Medicine Post-graduation in Structural and Functional Biology Federal University of São Paulo (UNIFESP) Department of Biology School of Biosciences Humanities and Exact Sciences São Paulo State University (UNESP) FAPESP: 2016/02012-4 FAPESP: 2017/09136-3 FAPESP: 2018/07895-7 CNPq: 308144/2014-7

Made available in DSpace on 2018-12-11T17:20:38Z (GMT). No. of bitstreams: 0 Previous issue date: 2018-10-01 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Zika virus (ZIKV) is a flavivirus that has been highly correlated with the development of neurological disorders and other malformations in newborns and stillborn fetuses after congenital infection. This association is supported by the presence of ZIKV in the fetal brain and amniotic fluid, and findings suggest that infection of the placental barrier is a critical step for fetal ZIKV infection in utero. Therefore, relevant models to investigate the interaction between ZIKV and placental tissues are essential for understanding the pathogenesis of Zika syndrome. In this report, we demonstrate that explant tissue from full-term human placentas sustains a productive ZIKV infection, though the results depend on the strain. Viral infection was found to be associated with pro-inflammatory cytokine expression and apoptosis of the infected tissue, and these findings confirm that placental explants are targets of ZIKV replication. We propose that human placental explants are useful as a model for studying ZIKV infection ex vivo. Department of Biology School of Biosciences Humanities and the Exact Sciences São Paulo State University (UNESP), São José do Rio Preto Federal University of São Paulo (UNIFESP) Brazilian Biosciences National Laboratory (LNBio) National Center for Research in Energy and Materials (CNPEM) Paulo de Góes Department of Microbiology Federal University of Rio de Janeiro (UFRJ) George Mason University Virology Research Laboratory Department of Dermatological Infectious and Parasitic Diseases São José do Rio Preto School of Medicine (FAMERP), São José do Rio Preto Department of Biology School of Biosciences Humanities and the Exact Sciences São Paulo State University (UNESP), São José do Rio Preto FAPESP: 2013/21719-3

Mayaro virus is a neglected tropical arbovirus that causes a mild, self-limited febrile syndrome, sometimes accompanied by a highly incapacitating arthralgia. First isolated in Trinidad and Tobago in 1954, it was reported in several countries within the tropical regions of South and Central America. Human infections are accidental spillover of the enzootic cycle. Little epidemiological data are available due to inadequate surveillance and the generic nature of clinical manifestations resulting in the misdiagnosis with other viral fevers. Despite its restricted distribution, Mayaro fever may become a public health issue due to their urbanization potential. Accurate epidemiological data are urgently needed to access the real distribution of this virus guiding public health policies better.

Yellow fever virus (YFV) replication is highly dependent on host cell factors. YFV NS4B is reported to be involved in viral replication and immune evasion. Here interactions between NS4B and human proteins were determined using a GST pull-down assay and analyzed using 1-DE and LC-MS/MS. We present a total of 207 proteins confirmed using Scaffold 3 Software. Cyclophilin A (CypA), a protein that has been shown to be necessary for the positive regulation of flavivirus replication, was identified as a possible NS4B partner. 59 proteins were found to be significantly increased when compared with a negative control, and CypA exhibited the greatest difference, with a 22-fold change. Fisher's exact test was significant for 58 proteins, and the p value of CypA was the most significant (0.000000019). The Ingenuity Systems software identified 16 pathways, and this analysis indicated sirolimus, an mTOR pathway inhibitor, as a potential inhibitor of CypA. Immunofluorescence and viral plaque assays showed a significant reduction in YFV replication using sirolimus and cyclosporine A (CsA) as inhibitors. Furthermore, YFV replication was strongly inhibited in cells treated with both inhibitors using reporter BHK-21-rep-YFV17D-LucNeoIres cells. Taken together, these data suggest that CypA-NS4B interaction regulates YFV replication. Finally, we present the first evidence that YFV inhibition may depend on NS4B-CypA interaction.

Ambientes hidricos localizados em centros urbanos sofrem intensas pressoes das atividades antropicas comprometendo sua qualidade. A criacao de parques urbanos constitui uma das principais estrategias utilizadas para minimizar esses impactos e atingir protecao e conservacao de ambientes naturais. Portanto, este trabalho tem como objetivo avaliar parâmetros microbiologicos e fisico-quimicos de aguas localizadas em quatro parques urbanos no DF, que fazem parte da unidade hidrografica do Lago Paranoa. As coletas ocorreram mensalmente nos periodos de outubro a dezembro de 2009 e marco a maio de 2010. Foram analisados os indicadores microbiologicos coliformes totais e termotolerantes, por metodo de substrato enzimatico (Colilert®) e fisico-quimicos temperatura, condutividade, OD e pH, atraves do aparelho multiparametro marca Hanna. Os resultados encontrados mostram que dos quatro parques, tres (Parques Aguas Claras, Parque Asa Sul e Parque Olhos D'agua) apresentaram coliformes termotolerantes em concentracoes crescentes nos meses de outubro a dezembro (entre 200 NMP/100 mL e 2.419,60 NMP/100 mL) e valores decrescentes em marco a maio (de 2.419,60 NMP/100 mL a 344,60NMP/100 mL), indicando possivel influencia da sazonalidade e de contribuicao difusa de poluicao. Ja no Parque Ezechias Heringer (Guara) a partir de dezembro o quantitativo desse indicador permaneceu constante com valor >2.419,6 NMP/100 mL, inferindo uma provavel contribuicao de poluicao pontual. Os parâmetros fisico-quimicos nao apresentaram variacoes significativas ao longo dos meses, mas foram expressivos na avaliacao da qualidade da agua do Parque Asa Sul.