ABOUT DENGUE
What is dengue fever?
dengue fever is a disease caused by a family of viruses that are transmitted by mosquitoes. It is an acute illness of sudden onset that usually follows a benign course with symptoms such as headache, fever, exhaustion, severe muscle and joint pain, swollen glands (lymphadenopathy), and rash. The presence (the “dengue triad”) of fever, rash, and headache (and other pains) is particularly characteristic of dengue. Other signs of dengue fever include bleeding gums, severe pain behind the eyes, and red palms and soles.
Dengue (pronounced DENG-gay) strikes people with low levels of immunity. Because it is caused by one of four serotypes of virus, it is possible to get dengue fever multiple times. However, an attack of dengue produces immunity for a lifetime to that particular serotype to which the patient was exposed.
Dengue goes by other names, including “breakbone” or “dandy fever.” Victims of dengue often have contortions due to the intense joint and muscle pain, hence the name breakbone fever. Slaves in the West Indies who contracted dengue were said to have dandy fever because of their postures and gait
Characteristics of dengue virus-infected peripheral blood mononuclear cell death that correlates with the severity of illness.
The Essay on Dengue Fever Bacteria Viruses Virus
... headache and a sore throat. Dengue fever is caused by aedes ... dengue fever, and polio. Ebola is a very dangerous virus that is caused by the ebola virus. The main symptoms consist of fever, weakness, muscle pain, ...
Abstract
The pathogenic mechanism of the severe form of dengue is complicated. Recent reports indicate that apoptotic death of various tissues or organs may be associated with vascular leakage, and ultimately leads to the death of DENV-infected patients. In the present study, we provide additional evidence supporting the detrimental role of apoptosis in DENV infection. A comparison of the rate of apoptosis in PBMCs isolated from patients suffering DF, a mild form of the disease, and the rate in patients with DHF, a life-threatening disease, revealed that PBMCs from DHF patients underwent apoptosis at a significantly higher rate than those suffering from DF alone. This suggests that the severity of natural DENV infection correlates with PBMC apoptosis. In addition, this cell death was induced not only by DENV itself, but also by the apoptotic activities of pro-inflammatory cytokines, such as TNF-alpha, and IL-1beta, that were upregulated in DHF patients. The death of these mononuclear cells that function in an innate immune system may explain the higher viral load in DHF patients than in DF patients. Interestingly, a gene expression profile pattern elucidated that apoptosis occurring during natural DENV infection involved mainly the extrinsic apoptosis pathway, which is mediated via both caspase-dependent and caspase-independent mechanisms. In conclusion, our data highlight the adverse effect of apoptosis induced by DENV and by pro-inflammatory cytokines during natural DENV infection.
