Literature review on Dengue Virus

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Literature review on Dengue Virus

Category: Biology

Subcategory: Cancer

Level: University

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Literature Review on Dengue Virus
According to the Global Burden of Diseases, Injuries, and Risk factors report, the occurrence of the dengue virus has amplified with a 610.87% from 1990 to 2013. Over these years, there have been over 390 million cases of the dengue virus reported globally on an annual basis (Stanway et al., 712). South Asia regions account for the largest part of the virus incidences being reported annually. With countries like India, Bangladesh, Indonesia, China, Vietnam, Thailand and Vietnam taking up the largest proportion of dengue fever virus cases being reported. The United States Department of Health and Human Services (Center for Disease Control and Prevention), describes the dengue virus as a mosquito-borne disease caused by four major viri identified as the (DENV-1, -2, -3 and -4) (Gubler, 1). The disease is transmitted by the Aedes mosquitoes in the local human environment. The infection of dengue virus increases the vascular permeability in the body of the host which results in circulatory failure and plasma leakages attributed to the increased vascular permeability.
Thein et al. (714), DHF infection is highly associated with increased vascular NO bioavailability which results in increased endothelial functions within the body of the host. In this case, the dengue virus infection results in peripheral arterial tonometry complications within the host’s body cells. Through an application of a longitudinal adult study, the authors report an increased vascular nitric oxide bioavailability in patients who were infected with the dengue hemorrhagic fever compared to other types of febrile diseases. Also, it is noted that the increased vascular nitric oxide as a result of the dengue virus infection results to an increased vascular permeability and impaired homeostasis in the hosts’ body cells (Thein et al., 711).
Dengue fever is highly linked to the development of the dengue hemorrhagic fever (DHF) which results in excessive bleeding and plasma leakage within the host body. Primary dengue virus infection in adults and children at their late stages of growth may develop to the dengue fever which is characterized by several symptoms which include, hemorrhagic manifestations, headache, myalgia, and retro-orbital pain (Srikiatkhachorn, 2). The case treatment of the dengue hemorrhagic fever is dependent on several factors which revolve around the bleeding signs and compromise of the circulatory systems which calls for supportive treatment. As a result of the infection, blood volume depletion occurs due to extensive bleeding, plasma leakage, poor oral intake and high fever which also results in increased levels of dehydration within the host’s body. At a significant level of hemorrhage fever infection, blood transfusion is a requirement (Rajapakse, 103). In other cases, there is a need to administer crystalloid fluid to regulate the patient’s blood pressure. Otherwise, the intravenous fluid treatment can be applied through careful medical procedures to maintain optimum blood circulation. In serious complications such as respiratory failure and pulmonary edema, an excessive fluid treatment medical procedure is more effective than the other methods based on the health condition of the patient (Srikiatkhachorn, 3). According to the World Health Organization (3), there is no specific treatment for the dengue virus. However, specialized medical care from experienced nurses and doctors with relevant knowledge on the effects and the progression of the dengue virus can save people infected suffering from the dengue hemorrhagic fever. The critical treatment aspect is to ensure that the patient’s body fluid is maintained at optimum levels.
Flaviviruses are the major cause of various forms of fever infections which include the dengue fever, yellow fever, West Nile virus, and the Japanese encephalitis. Among these diseases, the dengue fever has had the most significant impact on the humans’ health with more than 50 million each year and more than 20,000 deaths reported annually. All other forms of fever caused by these particular flaviviruses have vaccines. However, the dengue fever vaccine is yet to be discovered though there has been some positive research development on the possibility of getting a vaccine for the disease soon. The NS1 protein found in these flaviviruses responsible for the dengue fever has been the major hindrance towards the vaccine research development. The NS1 genes found in these form viruses are relatively homologous containing various oligomer forms such as the hexamer and dimer shapes. The multiple forms of the dengue flaviviruses are responsible for the viruses in the host’s immune system (Muller and Young, 193). Once infected by the dengue virus through the Aedes mosquitoes, the NS1 protein strand found in the flaviviruses is secreted through a dimerization process to three distinct regions in a human host cell; the infected cell surface, viral replication sites within the cell and the extracellular space. In this regions, the NS1 protein becomes a significant cofactor element towards its RNA viral replication within the host cells (Khromykh et al., 10274).
Blood circulation in the body is a complex biological process that involves several processes and interaction in the human body cells. In particular, patients suffering from dengue fever have their blood circulation becoming compromised as a result of the interactions between pericytes and endothelial in the human’s body vasculature. The vasculature stability is supported but the pericytes found in the newly formed blood vessels. Endothelial cells secrete a platelet-derived growth factor (PDGF) (Armulik et al., 514-516). A compromise on the pericyte coverage a result of hemorrhage in the blood vessels due to dengue fever causes abnormal and immature blood vessels within the host’s body. The dengue hemorrhagic fever is closely associated with endothelial cell dysfunction. The interaction between the human immune system and the virus antigen can lead to endothelial cell dysfunction thereby weakening the endothelial cell barrier integrity within the host’s cell. According to Srikiatkhachorn and James (162), the dengue virus infects the dendritic cells, monocytes, macrophages and endothelial cells which result in an increased viremia in the host’s body cells. On the surface of the endothelial cells, angiopoietin (ang)-1 and (ang)-2, VEGF and sVEgfr2 are present in the blood. At the early stages of the endothelium is not affected by the infection thereby the plasma leakage cannot be observed. However, successive infections increase the interaction of the endothelial cells with NS1 proteins a process that activates the complement system in the host’s body.
The changes in the endothelial cell’s interactions with the pericytes in the vasculature play a significant role in the emergence and the impact of dreadful human diseases in the host’s body. The endothelial cells are responsible for the preservation of functional capillaries in the body. As such, it leads to more complications to the hosts due to the alterations of the endothelial cells. These diseases include heart disease, cancer, peripheral vascular disease, venous thrombosis, stroke, diabetes, insulin resistance, tumor development, kidney failure, and multiple viral infections (Rajendran, 1057).

Works cited
Armulik, Annika, Alexandra Abramsson, and Christer Betsholtz. “Endothelial/pericyte interactions.” Circulation research 97.6 (2005): 512-523.
Gubler, Duane J., et al., eds. Dengue and dengue hemorrhagic fever. CABI, 2014.
Khromykh, Alexander A., et al. “Efficient trans-complementation of the flavivirus kunjin NS5 protein but not of the NS1 protein requires its coexpression with other components of the viral replicase.” Journal of Virology 73.12 (1999): 10272-10280.
Muller, David A., and Paul R. Young. “The flavivirus NS1 protein: molecular and structural biology, immunology, role in pathogenesis and application as a diagnostic biomarker.” Antiviral research 98.2 (2013): 192-208.
Rajapakse, Senaka, Chaturaka Rodrigo, and Anoja Rajapakse. “Treatment of dengue fever.” Infection and drug resistance 5 (2012): 103.
Rajendran, Peramaiyan, et al. “The vascular endothelium and human diseases.” International journal of biological sciences9.10 (2013): 1057.
Srikiatkhachorn, Anon, and James F. Kelley. “Endothelial cells in dengue hemorrhagic fever.” Antiviral research 109 (2014): 160-170.
Srikiatkhachorn, Anon. “Plasma leakage in dengue haemorrhagic fever.” Thrombosis and haemostasis 102.06 (2009): 1042-1049.
Stanaway, Jeffrey D., et al. “The global burden of dengue: an analysis from the Global Burden of Disease Study 2013.” The Lancet infectious diseases 16.6 (2016): 712-723.
Thein, Tun-Linn, et al. “Association between increased vascular nitric oxide bioavailability and progression to dengue hemorrhagic fever in adults.” The Journal of infectious diseases 212.5 (2015): 711-714.
World Health Organization. “Dengue and severe dengue.” (2014).

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