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Dengue Virus (dengue + virus)
Selected AbstractsDengue virus-specific suppressor T cells: current perspectivesFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2007Umesh C. Chaturvedi Abstract Dengue virus was the first microorganism that was shown to induce generation of antigen-specific suppressor T (TS) cells in mice. The cascade of the three generations of TS cells (TS1, TS2, TS3) and their secretary products, the suppressor factors (SF1, SF2), was delineated. The TS pathway was proposed to be protective through inhibition of the production of enhancing antibody, which may enhance the severity of dengue disease. The currently second most favoured mechanism of severe dengue disease is the ,cytokine tsunami'. During the last decade, suppressor/regulatory T cells have been studied in greater detail using modern techniques in various diseases, including viral infections. This brief review discusses the role of dengue-specific suppressor T cells in protection and/or induction of severe dengue disease in view of our current understanding of suppressor/regulatory T cells. [source] Cytokine cascade in dengue hemorrhagic fever: implications for pathogenesisFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2000U.C. Chaturvedi Abstract Dengue virus produces a mild acute febrile illness, dengue fever (DF) and a severe illness, dengue hemorrhagic fever (DHF). The characteristic feature of DHF is increased capillary permeability leading to extensive plasma leakage in serous cavities resulting in shock. The pathogenesis of DHF is not fully understood. This paper presents a cascade of cytokines, that in our view, may lead to DHF. The main feature is the early generation of a unique cytokine, human cytotoxic factor (hCF) that initiates a series of events leading to a shift from Th1-type response in mild illness to a Th2-type response resulting in severe DHF. The shift from Th1 to Th2 is regulated by the relative levels of interferon-gamma and interleukin (IL)-10 and between IL-12 and transforming growth factor-,, which showed an inverse relationship in patients with DF. [source] Development of a consensus microarray method for identification of some highly pathogenic virusesJOURNAL OF MEDICAL VIROLOGY, Issue 11 2009Kang Xiao-Ping Abstract Some highly pathogenic viruses, such as Chikungunya virus, Japanese encephalitis virus, Yellow fever virus, Dengue virus, Hanta virus, SARS-CoV, and H5N1 avian influenza virus can cause severe infectious diseases. However, the consensus method for detecting these viruses has not been well established. A rapid and sensitive microarray approach for detection of these viruses and a panel of specific probes covering nine genera and 16 virus species were designed. 70-mer oligonucleotides were used at the genus level and 50-mer oligonucleotides were at the species level, respectively. To decrease the interference of the host genome in hybridization, the consensus genus primers were designed and used to reverse transcribe only virus genome. The synthesis of the second strand was carried out with a random primer sequence (5,-GTTTCCCAGTAGGTCTCNNNNNNNN-3,). The amplified products were labeled and processed for microarray analyses. This microarray-based method used the highly conserved consensus primers to synthesize specifically the virus cDNA and could identify effectively Chikungunya virus, Japanese encephalitis virus, Yellow fever virus, Dengue virus, Tick borne encephalitis virus, and H5N1 avian influenza virus. Using this method, one unknown virus isolated from pig brain in Shanxi Province, China was identified. This method may have an important potential application for the diagnosis of virus infection. J. Med. Virol. 81:1945,1950, 2009. © 2009 Wiley-Liss, Inc. [source] Vascular endothelium: the battlefield of dengue virusesFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2008Atanu Basu Abstract Increased vascular permeability without morphological damage to the capillary endothelium is the cardinal feature of dengue haemorrhagic fever (DHF)/dengue shock syndrome (DSS). Extensive plasma leakage in various tissue spaces and serous cavities of the body, including the pleural, pericardial and peritoneal cavities in patients with DHF, may result in profound shock. Among various mechanisms that have been considered include immune complex disease, T-cell-mediated, antibodies cross-reacting with vascular endothelium, enhancing antibodies, complement and its products, various soluble mediators including cytokines, selection of virulent strains and virus virulence, but the most favoured are enhancing antibodies and memory T cells in a secondary infection resulting in cytokine tsunami. Whatever the mechanism, it ultimately targets vascular endothelium (making it a battlefield) leading to severe dengue disease. Extensive recent work has been done in vitro on endothelial cell monolayer models to understand the pathophysiology of vascular endothelium during dengue virus (DV) infection that may be translated to help understand the pathogenesis of DHF/DSS. The present review provides a broad overview of the effects of DV infection and the associated host responses contributing towards alterations in vascular endothelial cell physiology and damage that may be responsible for the DHF/DSS. [source] FasL/Fas pathway is involved in dengue virus induced apoptosis of the vascular endothelial cells,,JOURNAL OF MEDICAL VIROLOGY, Issue 8 2010Hongwu Liao Abstract The hallmark of the dengue hemorrhagic fever/dengue shock syndrome is hematologic abnormality. The pathogenesis of dengue hemorrhagic fever/dengue shock syndrome remains unknown. Our work showed that the dengue virus serotype-2 induced apoptosis in human umbilical vein endothelial cells. Fas (CD95), Tumor Necrosis Factor receptors, and Tumor Necrosis Factor-related apoptosis-inducing ligand receptors are the most common death receptors, which can induce apoptosis. Compared with the untreated human umbilical vein endothelial cells, Fas expression was increased both in the mRNA level and on the surface of infected human umbilical vein endothelial cells. FasL was expressed at similar levels on human umbilical vein endothelial cells over a course of dengue virus serotype-2 infection, but the expression in mRNA level was increased in infected human umbilical vein endothelial cells. It is possible that there is soluble FasL secreted from human umbilical vein endothelial cells in the supernatant. Tumor Necrosis Factor-related apoptosis-inducing ligand receptor 1 and Tumor Necrosis Factor receptors 1,2 were constantly very low, whereas Tumor Necrosis Factor-related apoptosis-inducing ligand receptors 2,4 decreased after dengue virus serotype-2 infection. This result suggested that dengue virus serotype-2 may inhibit Tumor Necrosis Factor-related apoptosis-inducing ligand receptors-induced apoptosis. The apoptotic rates in human umbilical vein endothelial cells were decreased upon the addition of caspase family inhibitors. In addition, activated caspase 8 and caspase 3 were also observed by Western blot following dengue virus serotype-2 infection. Thus, it is shown that the Fas/FasL pathway may participate in dengue virus-induced apoptosis of vascular endothelial cells in vitro. J. Med. Virol. 82:1392,1399, 2010. © 2010 Wiley-Liss, Inc. [source] Identification of a dengue virus-specific HLA-A*0201-restricted CD8+ T cell epitopeJOURNAL OF MEDICAL VIROLOGY, Issue 4 2010Jinsheng Wen Abstract In this study, a combination of epitope-prediction programs and in vitro assays was used to identify dengue virus (DENV)-specific CD8+ T cell epitopes. Peripheral blood mononuclear cells (PBMCs) isolated from patients who recovered from dengue fever were stimulated with candidate epitope peptides derived from DENV, which were predicted by using SYFPEITHI and RANKpep epitope-prediction programs. The IFN-, ELISpot results and the results of intracellular staining of IFN-, showed that peptides NS4b_40 (TLYAVATTI), E_256 (QEGAMHTAL), NS3_205 (LPAIVREAI), NS5_210 (SRNSTHEMY), and NS3_207 (AIVREAIKR) could induce the recall response of CD8+ T cells. Furthermore, the results of the MHC,peptide complex stabilization assay revealed that peptide NS4b_40 (TLYAVATTI) has a high affinity for HLA-A*0201 molecules. The IFN-, ELISpot results and staining of intracellular IFN-, confirmed that this peptide could induce high-level CD8+ T cell response in HLA-A*0201 positive PBMCs. Peptide NS4b_40 (TLYAVATTI) was identified as a novel DENV-specific HLA-A*0201-restricted CD8+ T cell epitope. J. Med. Virol. 82:642,648, 2010. © 2010 Wiley-Liss, Inc. [source] Travel-Associated Dengue Infections in the United States, 1996 to 2005JOURNAL OF TRAVEL MEDICINE, Issue 1 2010Hamish P. Mohammed PhD Background. As the incidence of dengue increases globally, US travelers to endemic areas may be at an increased risk of travel-associated dengue. Methods. Data from the US Centers for Disease Control and Prevention's laboratory-based Passive Dengue Surveillance System (PDSS) were used to describe trends in travel-associated dengue reported from January 1, 1996 to December 31, 2005. The PDSS relies on provider-initiated requests for diagnostic testing of serum samples via state health departments. A case of travel-associated dengue was defined as a laboratory-positive dengue infection in a resident of the 50 US states and the District of Columbia who had been in a dengue-endemic area within 14 days before symptom onset. Dengue infection was confirmed by serologic and virologic techniques. Results. One thousand one hundred and ninety-six suspected travel-associated dengue cases were reported,334 (28%) were laboratory-positive, 597 (50%) were laboratory-negative, and 265 (22%) were laboratory-indeterminate. The incidence of laboratory-positive cases varied from 1996 to 2005, but had an overall increase with no significant trend (53.5 to 121.3 per 108 US travelers, p = 0.36). The most commonly visited regions were the Caribbean, Mexico and Central America, and Asia. The median age of laboratory-positive cases was 37 years (range: <1 to 75 y) and 166 (50%) were male. Of the 334 laboratory-positive cases, 41 (12%) were hospitalized, and 2 (1%) died. Conclusions. Residents of the US traveling to dengue-endemic regions are at risk of dengue infection and need to be instructed on appropriate prevention measures prior to travel. Especially in light of the potential transmissibility of dengue virus via blood transfusion, consistent reporting of travel-associated dengue infections is essential. [source] Importation of Dengue by Soldiers Returning from East Timor to North Queensland, AustraliaJOURNAL OF TRAVEL MEDICINE, Issue 4 2002Scott Kitchener Background: Soldiers based in Townsville, Australia, returned from East Timor following peacekeeping operations during the wet season of 1999 to 2000. This represented the potential to import dengue virus into north Queensland, a dengue receptive area of Australia. This article seeks to outline the measures taken by the Australian Defence Force (ADF) to prevent local transmission and to present the outcomes. Methods: Soldiers returning to north Queensland were provided with education on dengue fever and in the fortnight before return, their living areas were subjected to intensive vector control measures, in order to reduce the risk of acquisition of dengue. They were further encouraged to present early with any febrile illness following their return to Townsville. Provisionally diagnosed dengue cases were notified to the state public health authorities immediately and cases were isolated until suitable vector control programs were implemented or the potentially viremic period exceeded. Serologic and virologic investigations were undertaken to identify the passage and probable serotype or confirm the presence and serotype of dengue virus. Results: Nine serologically confirmed cases of dengue were identified as viremic in north Queensland. Six cases were identified as arising from dengue serotype 2, two were from serotype 3, and one case was ill defined. No dengue cases have been reported in the local population 4 months following these ADF cases. Conclusions: Local outbreaks of dengue fever have occurred in north Queensland following the importation of dengue virus in returned travelers. The successful prevention of local transmission in these circumstances was contributed to by early notification of cases and prevention of transmission through isolation of cases and collaboration between ADF and state and local public health authorities in vector control. The management of potentially viremic returning service personnel represents a future challenge for the ADF. [source] Crystallization and preliminary X-ray diffraction analysis of West Nile virusACTA CRYSTALLOGRAPHICA SECTION F (ELECTRONIC), Issue 5 2010Bärbel Kaufmann West Nile virus, a human pathogen, is closely related to other medically important flaviviruses of global impact such as dengue virus. The infectious virus was purified from cell culture using polyethylene glycol (PEG) precipitation and density-gradient centrifugation. Thin amorphously shaped crystals of the lipid-enveloped virus were grown in quartz capillaries equilibrated by vapor diffusion. Crystal diffraction extended at best to a resolution of about 25,Å using synchrotron radiation. A preliminary analysis of the diffraction images indicated that the crystals had unit-cell parameters a , b , 480,Å, , = 120°, suggesting a tight hexagonal packing of one virus particle per unit cell. [source] Alternative infectious entry pathways for dengue virus serotypes into mammalian cellsCELLULAR MICROBIOLOGY, Issue 10 2009Eliana G. Acosta Summary The entry of two dengue virus (DENV) serotypes into Vero cells was analysed using biochemical inhibitors, dominant negative mutants of cellular proteins involved in endocytic pathways, fluorescence microscopy and infectivity determinations. By treatment with dansylcadaverine and chlorpromazine and overexpression of a dominant negative form of the Eps15 protein, a clathrin-mediated endocytosis for productive DENV-1 internalization into Vero cells was demonstrated whereas the infectious entry of DENV-2 in the same cell system was independent of clathrin. Treatment with the inhibitors nystatin and methyl-,-cyclodextrin, as well as transfection of Vero cells with dominant negative caveolin-1, had no effect on DENV-2 virus infection. It was also shown, by using the K44A mutant and the inhibitor dynasore, that dynamin was required for DENV-2 entry. Consequently, the infectious entry of DENV-2 into Vero cells occurs by a non-classical endocytic pathway independent of clathrin, caveolae and lipid rafts, but dependent on dynamin. By contrast, DENV-2 entry into A549 cells was clathrin-dependent, as previously reported in HeLa, C6/36 and BS-C-1 cells. Our results conclusively show, for the first time, a differential mode of infective entry for DENV-1 and DENV-2 into a common host cell, Vero cells, as well as alternative entry pathways for a given serotype, DENV-2, into different types of cells. [source] | |||||||||||||