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In the large Zika virus (ZIKV) epidemic that occurred in Brazil in 2015, the intrauterine fetal exposure to ZIKV was associated with a significant risk of developing microcephaly and neurological disorders in the infected infants. ZIKV-associated disease has since been reported in 24 countries in the Americas. At present, definitive evidence is lacking regarding the intrauterine co-exposure to ZIKV and other viral infections and whether the coinfection impacts the risk of acquiring either infection or disease severity. Here, we provide evidence of intrauterine exposure to both ZIKV and human immunodeficiency virus (HIV) infections, causing congenital Zika syndrome in an HIV-exposed uninfected infant. Clinical, imaging and laboratory examinations of the pregnant woman and the newborn were performed. Histopathology, ZIKV/HIV-specific immunoassays, and ultrastructural evaluation of the placenta were performed. The Zika-asymptomatic, HIV-positive pregnant woman underwent ultrasounds revealing fetal cerebral ventriculomegaly, microcephaly, and brain atrophy. Her baby girl was born small for gestational age and with the neurological sequelae of congenital Zika syndrome. The evaluation of the abnormally large term placenta revealed severe damage to the maternal decidua and chorionic villi, cells positive for ZIKV-specific antigens but not for HIV antigens, and intracellular membranous clusters of virus-like particles approximately 25 nm in diameter. The rapid progression and severity of the congenital Zika syndrome may be related to the uncontrolled HIV disease in the mother. The poor inflammatory response observed in the placenta may have reduced the inherent risk of mother-to-child transmission of HIV. [ABSTRACT FROM AUTHOR]

During the summer of 2002, Rio de Janeiro had a large epidemic of dengue fever; 288,245 cases were reported. A subset of 1,831 dengue hemorrhagic fever cases occurred. In this study, performed in the first half of 2002, samples from 1,559 patients with suspected cases of dengue infection were analyzed. From this total, 1,497 were obtained from patients with nonfatal cases, and 62 were obtained from patients with fatal cases. By the use of different methods, 831 (53.3%) cases, including 40 fatal cases, were confirmed as dengue infection. When virus identification was successful, dengue virus type 3 (DENV-3) was obtained in 99% of cases. Neurologic involvement was shown in 1 patient with encephalitis, confirmed by the detection of DENV-3 RNA in the cerebrospinal fluid. This explosive epidemic of DENV-3 was the most severe dengue epidemic reported in Brazil since dengue viruses were introduced in 1986. [ABSTRACT FROM AUTHOR]

In dengue virus (DENV) infection, complement system (CS) activation appears to have protective and pathogenic effects. In severe dengue fever (DF), the levels of DENV non-structural-1 protein and of the products of complement activation, including C3a, C5a and SC5b-9, are higher before vascular leakage occurs, supporting the hypothesis that complement activation contributes to unfavourable outcomes. The clinical manifestations of DF range from asymptomatic to severe and even fatal. Here, we aimed to characterise CS by their receptors or activation product, in vivo in DF patients and in vitro by DENV-2 stimulation on monocytes. In comparison with healthy controls, DF patients showed lower expression of CR3 (CD11b), CR4 (CD11c) and, CD59 on monocytes. The DF patients who were high producers of SC5b-9 were also those that showed more pronounced bleeding or vascular leakage. Those findings encouraged us to investigate the role of CS in vitro, using monocytes isolated from healthy subjects. Prior blocking with CR3 alone (CD11b) or CR3 (CD11b/CD18) reduced viral infection, as quantified by the levels of intracellular viral antigen expression and soluble DENV non-structural viral protein. However, we found that CR3 alone (CD11b) or CR3 (CD11b/CD18) blocking did not influence major histocompatibility complex presentation neither active caspase-1 on monocytes, thus probably ruling out inflammasome-related mechanisms. Although it did impair the secretion of tumour necrosis factor alpha and interferon alpha. Our data provide strategies of blocking CR3 (CD11b) pathways could have implications for the treatment of viral infection by antiviral-related mechanisms. [ABSTRACT FROM AUTHOR]

Background: Dengue displays a broad spectrum of clinical manifestations that may vary from asymptomatic to severe and even fatal features. Plasma leakage/hemorrhages can be caused by a cytokine storm induced by monocytes and dendritic cells during dengue virus (DENV) replication. Plasmacytoid dendritic cells (pDCs) are innate immune cells and in response to virus exposure secrete IFN-α and express membrane TRAIL (mTRAIL). We aimed to characterize pDC activation in dengue patients and their function under DENV-2 stimulation in vitro. Methods & Findings: Flow cytometry analysis (FCA) revealed that pDCs of mild dengue patients exhibit significantly higher frequencies of mTRAIL compared to severe cases or healthy controls. Plasma levels of IFN-α and soluble TRAIL are increased in mild compared to severe dengue patients, positively correlating with pDC activation. FCA experiments showed that in vitro exposure to DENV-2 induced mTRAIL expression on pDC. Furthermore, three dimension microscopy highlighted that TRAIL was relocalized from intracellular compartment to plasma membrane. Chloroquine treatment inhibited DENV-2-induced mTRAIL relocalization and IFN-α production by pDC. Endosomal viral degradation blockade by chloroquine allowed viral antigens detection inside pDCs. All those data are in favor of endocytosis pathway activation by DENV-2 in pDC. Coculture of pDC/DENV-2-infected monocytes revealed a dramatic decrease of antigen detection by FCA. This viral antigens reduction in monocytes was also observed after exogenous IFN-α treatment. Thus, pDC effect on viral load reduction was mainly dependent on IFN-α production Conclusions: This investigation characterizes, during DENV-2 infection, activation of pDCs in vivo and their antiviral role in vitro. Thus, we propose TRAIL-expressing pDCs may have an important role in the outcome of disease. [ABSTRACT FROM AUTHOR]

The article offers information on the clinical experience from the Reference Center of Dengue (RCD), a healthcare center providing assistance to patients with dengue, in Brazil. It mentions that dengue is initiated by several clinical signs including fever, prostration and myalgia. It informs that after the onset of clinical signs, various warning signs of hemorrhagic dengue appear in severe cases such as abdominal pain, persistent vomiting and hypotension. It also discusses several positive aspects for the RCD concerning dengue eradication including centralization of information, continuing epidemiological surveillance and monitoring of patients, thus avoiding deaths.

Dengue is an acute febrile illness with a wide spectrum of signs and symptoms ranging from mild to severe forms characterized by plasma leakage that can be fatal. NK cells are one of the main effectors in early infection and may play an important role in dengue pathogenesis. We investigated NK cell involvement during dengue infection. A higher frequency of NK cell subsets and TRAIL+NK cells was found in mild DF cases when compared to that in severe cases or healthy donors. NK activation markers such as CD107a and TLR3 were upregulated in patients' cells compared to those in healthy donors. In addition, IL12 related to NK cell activation were upregulated in mild DF cases. In vitro PBMC culture models show that DENV-stimulated and IFN α -stimulated NK cells were able to express TRAIL, suggesting an indirect activation of cells, regarding TRAIL expression. Type I IFN receptor blockage on DENV-stimulated PBMCs showed TRAIL expression on NK cells is partially IFN α dependent. In addition, during PBMC stimulation, TRAIL expression on NK cells was inversely correlated with DENV-positive monocytes. Therefore, we observed DENV-induced activation of NK cell populations. A higher activation of NK cells would promote limited viral spread, resulting in decreased inflammatory response, contributing to protection against dengue severity.

The objective of this study was to evaluate the impact of dengue virus infection on liver function by measuring aminotransferase in blood samples from patients serologically diagnosed by according to two MAC-ELISA protocols. Degrees of liver damage were classified according to aminotransferase levels: grade A--normal enzyme levels; grade B--increased levels of at least one of the enzymes; grade C--increased, with at least one of the enzymes being at levels higher than three times the upper reference values; grade D--acute hepatitis, with aminotransferase levels at least ten times their normal values. Of the 169 serologically confirmed cases of dengue at the dengue referral center in Campos dos Goytacazes in the state of Rio de Janeiro, Brazil, 65.1% had abnormal aminotransferase levels: 81 cases being classified as grade B, 25 as grade C and 3 as grade D. A further 34.9% of cases had normal enzyme levels and were classified as grade A. Liver damage is a common complication of dengue infection and aminotransferase levels are a valuable marker for monitoring these cases.

Dengue fever is the most important arboviral infection in the world, with an estimated 100 million cases per year and 2.5 billion people at risk. Encephalopathy is a rare complication of dengue virus infection and may occur as a consequence of intracranial hemorrhage, cerebral edema, hyponatremia, cerebral anoxia, fulminant hepatic failure with portosystemic encephalopathy, microcapillary hemorrhage or release of toxic products. We report a rare case of hemorrhagic encephalopathy in dengue shock syndrome caused by type 3 dengue virus.

Objective: To determine the prevalence of dyslipidemias in adults in the city of Campos dos Goytacazes, in the Brazilian state of Rio de Janeiro, and to identify its relation to risk factors., Methods: Cross-sectional, population-based, observational study with sampling through conglomerates and stratified according to socioeconomic levels, sex, and age, with 1,039 individuals. Risk factors, familial history, blood pressure, anthropometric measurements, glucose, triglycerides and cholesterol were determined., Results: The following prevalences were observed: of dyslipidemias 24.2%; of hypercholesterolemia, 4.2%; of elevated LDL-C, 3.5%; of low HDL-C, 18.3%; and of hypertriglyceridemia, 17.1%. The following mean levels were observed: cholesterol, 187.6 +/- 33.7 mg/dL; LDL-C, 108.7 +/- 26.8 mg/dL; HDL-C, 48.5 +/- 7.7 mg/dL; and triglycerides, 150.1 +/- 109.8 mg/dL. The following variables showed a positive correlation with dyslipidemia: increased age (P<0.001), male sex (P<0.001), low familial income (P<0.001), familial history (P<0.01), overweight/obesity (P<0.001), waist measure (P<0.001), high blood pressure (P<0.001), and diabetes mellitus (P<0.001). The following variables had no influence on dyslipidemias: ethnicity, educational level, smoking habits, and sedentary lifestyle., Conclusion: The frequency of lipid changes in the population studied was high, suggesting that measures for the early diagnosis should be taken, in association with implementation of programs for primary and secondary prevention of atherosclerosis.

Dengue fever is the most frequent arbovirus disease in the world and the most important one in terms of morbidity and mortality. Atypical manifestations of dengue have become commonplace during the last few years, including hepatic damage, which manifests mainly by pain in the right hypochondrium and an increase in the levels of aminotransferases. We describe a case of acute hepatitis in a patient with Dengue Shock Syndrome Grade III. We analyzed the clinical and laboratory aspects of this atypical complication of dengue as well as the differential diagnoses.