Dengue and Dengue Hemorrhagic Fever

Division of Vector-Borne Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado 80522, USA.
Clinical Microbiology Reviews (Impact Factor: 17.41). 08/1998; 11(3):480-96. DOI: 10.1016/S1045-1870(97)80003-9
Source: PubMed


Dengue fever, a very old disease, has reemerged in the past 20 years with an expanded geographic distribution of both the viruses and the mosquito vectors, increased epidemic activity, the development of hyperendemicity (the cocirculation of multiple serotypes), and the emergence of dengue hemorrhagic fever in new geographic regions. In 1998 this mosquito-borne disease is the most important tropical infectious disease after malaria, with an estimated 100 million cases of dengue fever, 500,000 cases of dengue hemorrhagic fever, and 25,000 deaths annually. The reasons for this resurgence and emergence of dengue hemorrhagic fever in the waning years of the 20th century are complex and not fully understood, but demographic, societal, and public health infrastructure changes in the past 30 years have contributed greatly. This paper reviews the changing epidemiology of dengue and dengue hemorrhagic fever by geographic region, the natural history and transmission cycles, clinical diagnosis of both dengue fever and dengue hemorrhagic fever, serologic and virologic laboratory diagnoses, pathogenesis, surveillance, prevention, and control. A major challenge for public health officials in all tropical areas of the world is to develop and implement sustainable prevention and control programs that will reverse the trend of emergent dengue hemorrhagic fever.

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Available from: Duane Gubler, Dec 11, 2015
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    • "Dengue is an arthropod borne febrile illness that is transmitted mainly by the bite of infected Aedes mosquitoes. Dengue virus (DENV) belongs to the family Flaviviridae and consists of four serotypes (DENV 1-4)[1] that cause a disease that may result in a mild dengue fever with or without warning signs or severe dengue[2]. Dengue fever usually presents with high fever, severe headache, myalgia, arthralgia, skin rashes, retro-orbital pain, leucopenia and thrombocytopenia which lead to respiratory distress, hemorrhage, organ impairment. "
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    ABSTRACT: Objective: To determine the burden of dengue in the patients visiting National Public Health Laboratory, Kathmandu. Methods: A cross sectional study was carried out at National Public Health Laboratory, Kathmandu from May to December, 2013. Serum samples were collected from patients suspected of dengue virus infection and tested by ELISA. Results: Among 266 patients suspected of dengue virus infection, 45 (16.9%) showed antidengue immunoglobulin M antibodies in serum. Males and economically active people were more infected and the maximum number of cases was during the month of October. Conclusions: This study revealed that the proportion of dengue was more in Kathmandu, especially among the economically active males. So, the control measures should be initiated targeting these groups of people.
    Full-text · Article · Feb 2015 · Asian Pacific Journal of Tropical Medicine
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    • "Dengue virus (DENV), a member of the Flaviviridae family, is transmitted to humans by mosquitoes of the Aedes genus. Dengue disease is a major emerging health problem in the world and the severe form of the infection and the co-circulation of different virus serotypes increases the frequency of epidemics (Gubler, 1998). In humans, DENV infection can cause a flu-like syndrome, which can evolve to a severe and sometimes fatal illness known as dengue hemorrhagic fever and shock syndrome (Guzman et al., 2006). "
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    ABSTRACT: tMicroRNAs (miRNAs) constitute an important class of non-coding RNA implicated in gene expression reg-ulation. More than 1900 miRNA molecules have been identified in humans and their modulation duringviral infection and it is recognized to play a role in latency regulation or in establishing an antiviral state.The liver cells are targets during DENV infection, and alteration of liver functions contributes to severedisease. In this work the miRNAs expression profile of the human hepatoma cell line, Huh-7, infected withDENV-2 was determined using microarray and real-time PCR. Let-7c is one of the miRNAs up-regulatedduring DENV infection in the hepatic Huh-7 as well as in the macrophage-monocytic cell line U937-DC-SIGN. Let-7c overexpression down-regulates both DENV-2 and DENV-4 infection. Additionally, we foundthat the transcription factor BACH1, a let-7c target, is also down-regulated during DENV infection. Inaccordance with this finding, HO-1, the main responsive factor of BACH1 was found up-regulated. Theup-regulation of HO-1 may contribute to the stress oxidative response in infected cells
    Full-text · Article · Jan 2015 · Virus Research
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    • "DENV infection causes a spectrum of illnesses ranging from acute febrile episode, known as dengue fever (DF), to the life-threatening DHF, which can occur in both primary and secondary infections, but is usually found in secondary infection, especially with different serotypes from the primary infection. DHF consists of serious complications, such as plasma leakage, hemorrhage, and multiple organ failure, and may lead to hypovolemic shock, known as DSS (Gubler, 1998; Halstead, 1988; Halstead, 2007). DENV infection associates with a variety of renal disorders (Lizarraga and Nayer, 2014). "
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    ABSTRACT: Dengue virus (DENV) infection associates with renal disorders. Patients with dengue hemorrhagic fever and acute kidney injury have a high mortality rate. Increased levels of cytokines may contribute to the pathogenesis of DENV-induced kidney injury. Currently, molecular mechanisms how DENV induces kidney cell injury has not been thoroughly investigated. Excessive cytokine production may involve in this process. Using human cytokine RT(2) Profiler PCR array, 14 genes including IP-10, RANTES, IL-8, CXCL-9 and MIP-1β were up-regulated more than 2folds in DENV-infected HEK 293 cells compared to that of mock-infected HEK 293 cells. In the present study, RANTES was suppressed by the NF-κB inhibitor, compound A (CpdA), in DENV-infected HEK 293 cells implying the role of NF-κB in RANTES expression. Chromatin immunoprecipitation (ChIP) assay showed that NF-κB binds more efficiently to its binding sites on the RANTES promoter in NS5-transfected HEK 293 cells than in HEK 293 cells expressing the vector lacking NS5. To further examine whether the NS5-activated RANTES promoter is mediated through NF-κB, the two NF-κB binding sites on the RANTES promoter were mutated and this promoter was coupled to the luciferase cDNA. The result showed that when both binding sites of NF-κB in the RANTES promoter were mutated, the ability of NS5 to induce the luciferase activity was significantly decreased. Therefore, DENV NS5 activates RANTES production by increasing NF-κB binding to its binding sites on the RANTES promoter. Copyright © 2014 Elsevier B.V. All rights reserved.
    Full-text · Article · Dec 2014 · Virus Research
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