scholarly journals The Battle between Infection and Host Immune Responses of Dengue Virus and Its Implication in Dengue Disease Pathogenesis

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Peifang Sun ◽  
Tadeusz J. Kochel
Keyword(s):  
Dengue Virus ◽  
Adaptive Immunity ◽  
Inflammatory Responses ◽  
Rna Virus ◽  
Dengue Shock Syndrome ◽  
Hemorrhagic Fever ◽  
Cell Types ◽  
Long Term Memory ◽  
Dengue Disease ◽  
Host Immune Responses

Dengue virus (DENV) is a mosquito-transmitted single stranded RNA virus belonging to genusFlavivirus. The virus is endemic in the tropical and subtropical countries of the world, causing diseases classified according to symptoms and severity (from mild to severe) as dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. Among a variety of human cell types targeted by DENV, monocytes, macrophages, and dendritic cells are members of innate immunity, capable of mounting rapid inflammatory responses. These cells are also major antigen presenting cells, responsible for activating the adaptive immunity for long-term memory. This paper is an overview of the current understanding of the following mutually affected aspects: DENV structure, viral infectivity, cellular receptors, innate immune response, and adaptive immunity.

scholarly journals Roles for Endothelial Cells in Dengue Virus Infection

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Nadine A. Dalrymple ◽  
Erich R. Mackow
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Capillary Permeability ◽  
Virus Disease ◽  
Dengue Shock Syndrome ◽  
Hemorrhagic Fever ◽  
Dengue Virus Infection ◽  
Barrier Functions ◽  
Dengue Disease ◽  
Primary Fluid

Dengue viruses cause two severe diseases that alter vascular fluid barrier functions, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). The endothelium is the primary fluid barrier of the vasculature and ultimately the effects of dengue virus infection that cause capillary leakage impact endothelial cell (EC) barrier functions. The ability of dengue virus to infect the endothelium provides a direct means for dengue to alter capillary permeability, permit virus replication, and induce responses that recruit immune cells to the endothelium. Recent studies focused on dengue virus infection of primary ECs have demonstrated that ECs are efficiently infected, rapidly produce viral progeny, and elicit immune enhancing cytokine responses that may contribute to pathogenesis. Furthermore, infected ECs have also been implicated in enhancing viremia and immunopathogenesis within murine dengue disease models. Thus dengue-infected ECs have the potential to directly contribute to immune enhancement, capillary permeability, viremia, and immune targeting of the endothelium. These effects implicate responses of the infected endothelium in dengue pathogenesis and rationalize therapeutic targeting of the endothelium and EC responses as a means of reducing the severity of dengue virus disease.

scholarly journals Dengue Immunopathogenesis: A Crosstalk between Host and Viral Factors Leading to Disease: Part I - Dengue Virus Tropism, Host Innate Immune Responses, and Subversion of Antiviral Responses

2020 ◽  
Author(s):  
Henry Puerta-Guardo ◽  
Scott B. Biering ◽  
Eva Harris ◽  
Norma Pavia-Ruz ◽  
Gonzalo Vázquez-Prokopec ◽  
...  
Keyword(s):  
Dengue Virus ◽  
Nonstructural Protein ◽  
Secondary Infection ◽  
Hypovolemic Shock ◽  
Clinical Manifestations ◽  
Dengue Shock Syndrome ◽  
Hemorrhagic Fever ◽  
Innate Immune ◽  
Vascular Leak ◽  
Dengue Disease

Dengue is the most prevalent emerging mosquito-borne viral disease, affecting more than 40% of the human population worldwide. Many symptomatic dengue virus (DENV) infections result in a relatively benign disease course known as dengue fever (DF). However, a small proportion of patients develop severe clinical manifestations, englobed in two main categories known as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Secondary infection with any of the four dengue virus serotypes (DENV1, -2, -3, and -4) is a risk factor to develop severe forms of dengue disease. DSS is primarily characterized by sudden and abrupt endothelial dysfunction, resulting in vascular leak and organ impairment, which may progress to hypovolemic shock and death. Severe DENV disease (DHF/DSS) is thought to follow a complex relationship between distinct immunopathogenic processes involving host and viral factors, such as the serotype cross-reactive antibody-dependent enhancement (ADE), the activation of T cells and complement pathways, the phenomenon of the cytokine storm, and the newly described viral toxin activity of the nonstructural protein 1 (NS1), which together play critical roles in inducing vascular leak and virus pathogenesis. In this chapter that is divided in two parts, we will outline the recent advances in our understanding of DENV pathogenesis, highlighting key viral-host interactions and discussing how these interactions may contribute to DENV immunopathology and the development of vascular leak, a hallmark of severe dengue. Part I will address the general features of the DENV complex, including the virus structure and genome, epidemiology, and clinical outcomes, followed by an updated review of the literature describing the host innate immune strategies as well as the viral mechanisms acting against and in favor of the DENV replication cycle and infection.

scholarly journals Clinical profile of dengue fever infection in patients admitted in NC Medical College, Haryana in the year 2019

2020 ◽  
Vol 8 (8) ◽  
pp. 3027
Author(s):  
Mohd Y. Shah ◽  
Faisal Y. Shah ◽  
Ifrah S. Kitab ◽  
Faizan Y. Shah
Keyword(s):  
Dengue Virus ◽  
Dengue Fever ◽  
Dengue Hemorrhagic Fever ◽  
Clinical Symptoms ◽  
Wide Spectrum ◽  
Dengue Shock Syndrome ◽  
Hemorrhagic Fever ◽  
Clinical Profile ◽  
Host Immune Responses ◽  
Medical College

Background: Dengue infections can result in a wide spectrum of disease severity ranging from an influenza-like illness (dengue fever; DF) to the life-threatening dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). The study was aimed to compare the clinical profile of all patients diagnosed with dengue viral infection at NCMC.Methods: This retrospective study included 24 patients infected with dengue virus, aged 19 years to 45 years. Laboratory and haematological data were included.Results Peak of infection occurred in November 2019 and no cases were recorded in October 2019. Common clinical symptoms were fever, joint pains, headache and rash. Common haematological abnormalities were thrombocytopenia. All patients survived. There was no case of dengue hemorrhagic fever or dengue shock syndrome.Conclusions: Significant differences in the clinical profile is possibly because of infection with different serotypes of dengue virus (DENV), concurrent/sequential infection of more than one serotype, and differences in host immune responses associated with host genetic variations.

scholarly journals Clinical profile of dengue fever infection in patients admitted in NCMC medical college, Panipat, Haryana, India

2018 ◽  
Vol 6 (3) ◽  
pp. 878
Author(s):  
Mohd Younus Shah ◽  
Faisal Y. Shah ◽  
Faizan Y. Shah ◽  
Saurabh Satya
Keyword(s):  
Dengue Virus ◽  
Dengue Fever ◽  
Dengue Hemorrhagic Fever ◽  
Clinical Symptoms ◽  
Wide Spectrum ◽  
Dengue Shock Syndrome ◽  
Hemorrhagic Fever ◽  
Clinical Profile ◽  
Host Immune Responses ◽  
Medical College

Background: Dengue infections can result in a wide spectrum of disease severity ranging from an influenza-like illness (dengue fever; DF) to the life-threatening dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). The study was aimed to compare the clinical profile of all patients diagnosed with dengue viral infection at NCMC.Methods: This retrospective study included 136 patients infected with dengue virus, age 2 years to 68 years. Laboratory and haematological data were included.Results: Peak of infection occurred in Nov. 2017 and least number of cases were recorded in September 2017. Common clinical symptoms were fever, headache and myalgia. Common haematological abnormalities were thrombocytopenia and leucopoenia. All patients survived. There was no case of dengue hemorrhagic fever or dengue shock syndrome.Conclusions: Significant differences in the clinical profile is possibly because of infection with different serotypes of dengue virus (DENV), concurrent/sequential infection of more than one serotype, and differences in host immune responses associated with host genetic variations.

scholarly journals Melatonin Inhibits Dengue Virus Infection via the Sirtuin 1-Mediated Interferon Pathway

Viruses ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 659
Author(s):  
Atthapan Morchang ◽  
Shilu Malakar ◽  
Kanchanaphan Poonudom ◽  
Sansanee Noisakran ◽  
Pa-thai Yenchitsomanus ◽  
...  
Keyword(s):  
Dengue Virus ◽  
Production Cross ◽  
Dengue Shock Syndrome ◽  
Hemorrhagic Fever ◽  
Cell Types ◽  
Denv Infection ◽  
Sirtuin 1 ◽  
Natural Hormone ◽  
New Strategy ◽  
Post Entry

Dengue virus (DENV) is the causative pathogen in the life-threatening dengue hemorrhagic fever and dengue shock syndrome. DENV is transmitted to humans via the bite of an infected Aedes mosquito. Approximately 100 million people are infected annually worldwide, and most of those live in tropical and subtropical areas. There is still no effective drug or vaccine for treatment of DENV infection. In this study, we set forth to investigate the effect of melatonin, which is a natural hormone with multiple pharmacological functions, against DENV infection. Treatment with subtoxic doses of melatonin dose-dependently inhibited DENV production. Cross-protection across serotypes and various cell types was also observed. Time-of-addition assay suggested that melatonin exerts its influence during the post-entry step of viral infection. The antiviral activity of melatonin partly originates from activation of the sirtuin pathway since co-treatment with melatonin and the sirtuin 1 (SIRT1) inhibitor reversed the effect of melatonin treatment alone. Moreover, melatonin could modulate the transcription of antiviral genes that aid in suppression of DENV production. This antiviral mechanism of melatonin suggests a possible new strategy for treating DENV infection.

scholarly journals Cells in Dengue Virus Infection In Vivo

2010 ◽  
Vol 2010 ◽  
pp. 1-15 ◽  
Author(s):  
Sansanee Noisakran ◽  
Nattawat Onlamoon ◽  
Pucharee Songprakhon ◽  
Hui-Mien Hsiao ◽  
Kulkanya Chokephaibulkit ◽  
...  
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Emerging Infectious Diseases ◽  
Dengue Shock Syndrome ◽  
Hemorrhagic Fever ◽  
Severe Dengue ◽  
Dengue Virus Infection ◽  
Dengue Disease

Dengue has been recognized as one of the most important vector-borne emerging infectious diseases globally. Though dengue normally causes a self-limiting infection, some patients may develop a life-threatening illness, dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). The reason why DHF/DSS occurs in certain individuals is unclear. Studies in the endemic regions suggest that the preexisting antibodies are a risk factor for DHF/DSS. Viremia and thrombocytopenia are the key clinical features of dengue virus infection in patients. The amounts of virus circulating in patients are highly correlated with severe dengue disease, DHF/DSS. Also, the disturbance, mainly a transient depression, of hematological cells is a critical clinical finding in acute dengue patients. However, the cells responsible for the dengue viremia are unresolved in spite of the intensive efforts been made. Dengue virus appears to replicate and proliferate in many adapted cell lines, but these in vitro properties are extremely difficult to be reproduced in primary cells or in vivo. This paper summarizes reports on the permissive cells in vitro and in vivo and suggests a hematological cell lineage for dengue virus infection in vivo, with the hope that a new focus will shed light on further understanding of the complexities of dengue disease.

scholarly journals UPDATE MANAGEMENT OF DENGUE COMPLICATION IN PEDIATRIC

2015 ◽  
Vol 2 (1) ◽  
pp. 1
Author(s):  
Soegeng Soegijanto
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Clinical Performance ◽  
Kidney Injury ◽  
Dengue Shock Syndrome ◽  
Hemorrhagic Fever ◽  
Liver Involvement ◽  
Dengue Virus Infection ◽  
Important Health ◽  
Grade Iii

Dengue virus infection is one of the important health problems in Indonesia, although the mortality rate has been decreased but many dengue shock syndrome cases is very difficult to be solving handled. It might be due to nature course of dengue virus infection is very difficult to predict of the earlier time of severity occur. THE AIM To get idea to make update management of dengue complication in pediatric. MATERIAL AND METHOD Data were compiled from Dr. Soetomo Hospital Surabaya in 2009. The diagnosis of all cases was based on criteria WHO 1997 and PCR examination in Institute Tropical Disease for identified serotype of dengue virus infection. The unusual cases of dengue virus infection were treated following the new WHO protocol in 2009. RESULT There were only 3 cases with serotype DEN 1, consisted 2 cases had age 1–4 years and 1 had age 5–14 years. 2 cases showed a severe clinical performance as dengue shock syndrome and 1 case showed as unusual case of dengue virus infection. Three report cases of: a. Dengue hemorrhagic fever grade III which liver involvement and had bilateral pleural effusion; b. Dengue hemorrhagic grade III with liver involvement and encephalopathy; c. Dengue hemorrhagic grade III with liver involvement acute kidney injury, myocardial involvement and encephalopathy. All the patients were treated according to new edition WHO protocol and all of the involving organ recovered along with the improvement of the disease. CONCLUSION Update management of dengue complication pediatric should be learned carefully used for helping unusual cases of dengue virus infection.

scholarly journals Recent Advances in DENV Receptors

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Shuyu Fang ◽  
Yanhua Wu ◽  
Na Wu ◽  
Jing Zhang ◽  
Jing An
Keyword(s):  
Endothelial Cells ◽  
Dengue Shock Syndrome ◽  
Hemorrhagic Fever ◽  
Infection Risk ◽  
Target Cells ◽  
Virus Binding ◽  
Dengue Disease ◽  
High Infection ◽  
Key Factor ◽  
Serious Disease

Dengue is an old disease caused by the mosquito-borne dengue viruses (DENVs), which have four antigenically distinct serotypes (DENV1–4). Infection by any of them can cause dengue fever (DF) and/or a more serious disease, that is, dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS). In recent decades, incidence of dengue disease has increased 30-fold, putting a third to half of the world’s population living in dengue-endemic areas at high infection risk. However, the pathogenesis of the disease is still poorly understood. The virus binding with its host cell is not only a first and critical step in their replication cycle but also a key factor for the pathogenicity. In recent years, there have been significant advances in understanding interactions of DENVs with their target cells such as dendritic cells (DC), macrophages, endothelial cells, and hepatocytes. Although DENVs reportedly attach to a variety of receptors on these cells, consensus DENV receptors have not been defined. In this review, we summarize receptors for DENVs on different cells identified in recent years.

scholarly journals Polyamines and Hypusination Are Required for Ebolavirus Gene Expression and Replication

mBio ◽  
2016 ◽  
Vol 7 (4) ◽  
Author(s):  
Michelle E. Olsen ◽  
Claire Marie Filone ◽  
Dan Rozelle ◽  
Chad E. Mire ◽  
Krystle N. Agans ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Virus ◽  
Hemorrhagic Fever ◽  
Cell Types ◽  
Host Protein ◽  
Initiation Factor ◽  
Virus Protein ◽  
Human Pathogens ◽  
Viral Polymerase ◽  
And Function

ABSTRACTEbolavirus (EBOV) is an RNA virus that is known to cause severe hemorrhagic fever in humans and other primates.EBOV successfully enters and replicates in many cell types. This replication is dependent on the virus successfully coopting a number of cellular factors. Many of these factors are currently unidentified but represent potential targets for antiviral therapeutics. Here we show that cellular polyamines are critical for EBOV replication. We found that small-molecule inhibitors of polyamine synthesis block gene expression driven by the viral RNA-dependent RNA polymerase. Short hairpin RNA (shRNA) knockdown of the polyamine pathway enzyme spermidine synthase also resulted in reduced EBOV replication. These findings led us to further investigate spermidine, a polyamine that is essential for the hypusination of eukaryotic initiation factor 5A (eIF5A). Blocking the hypusination of eIF5A (and thereby inhibiting its function) inhibited both EBOV gene expression and viral replication. The mechanism appears to be due to the importance of hypusinated eIF5A for the accumulation of VP30, an essential component of the viral polymerase. The same reduction in hypusinated eIF5A did not alter the accumulation of other viral polymerase components. This action makes eIF5A function an important gate for proper EBOV polymerase assembly and function through the control of a single virus protein.IMPORTANCEEbolavirus (EBOV) is one of the most lethal human pathogens known. EBOV requires host factors for replication due to its small RNA genome. Here we show that the host protein eIF5A in its activated form is necessary for EBOV replication. We further show that the mechanism is through the accumulation of a single EBOV protein, VP30. To date, no other host proteins have been shown to interfere with the translation or stability of an EBOV protein. Activated eIF5A is the only protein in the cell known to contain the specific modification of hypusine; therefore, this pathway is a target for drug development. Further investigation into the mechanism of eIF5A interaction with VP30 could provide insight into therapeutics to combat EBOV.

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