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Mbocytes, and endothelial cells[43]. NS1 is a glycoprotein that is secreted by infected cells, heavily present in patient serum supernatants, lacks a membrane spanning motif, but is not, itself, present in the virus. NS1 is known to be a major immune target and high concentrations of antiNS1 antibodies have been found in severe disease in patient studies[44]. When cells are exposed to NS1 antibod
Izes DHF/DSS are regulated by Complement proteins and associated anaphylatoxins. These three systems both interact and reinforce each other to create a potentially life threatening situation during a Dengue infection.Antibodies Antibody Dependent Enhancement (ADE) has been proposed to be a mechanism by which the immune system may enhance viral pathogenesis[7]. When monkeys were passively immunize
Egins with dengue infection of dendritic cells that, in turn, promiscuously activates T cells. T cells during a dengue infection have prolific and cross reactive effector functions in addition to producing copious amounts of cytokines that feature prominently in cases of DHF/DSS. A second component in immune enhancement is Antibody Dependant Enhancement (ADE). Heterologus non-neutralizing antibod
Are unaffected by the virus. There are yet questions unanswered and the virus continues to spread unabated. However these immune components are several key elements attractive targets for study that hopefully can advance the field of research.12.13. 14. 15. 16.Competing interestsThe author declares that they have no competing interests.Authors' informationsDavid Gentry Nielsen was born 27, Septem
Om neutrophils, eosinophiles, and basophiles. C3a and C5a act on specific receptors to produce local inflammatory responses and when secreted in concentrations high enough to invoke a general systemic response, they cause circulatory collapse similar to an IgE mediated allergic response. ATs modulate the secretion of IL-6, and TNF from B cells and serve as potent chemoattractants[52]. C5a also wo
Reactive antibodies activate complement still further. The increase in alternative complement proteins, complement receptors and C protein all facilitate a positive feedback loop that can have dangerous consequences in a dengue infected patient.ConclusionThree immune components interact to produce a confluence of symptoms that define DHF/DSS. Dengue virus initially infects immature dendritic cell
Ivation is greatly enhanced. When they added purified NS1 protein to normal or convalescent sera they found synonymous results with NS1 activating complement and complement activation being synergized by anti-dengue antibodies. While NS1 could clearly activate complement in the fluid phase it was unable activate complement when stably expressed on the surface of cells. However, when patient sampl
Om neutrophils, eosinophiles, and basophiles. C3a and C5a act on specific receptors to produce local inflammatory responses and when secreted in concentrations high enough to invoke a general systemic response, they cause circulatory collapse similar to an IgE mediated allergic response. ATs modulate the secretion of IL-6, and TNF from B cells and serve as potent chemoattractants[52]. C5a also wo
Helial cells, smooth muscles cells, and activated T-cells, but, interestingly, not na e T-cells. C5aR also activates a number of downstream signaling pathways including PI3K- (Phosophoinosital -3 Kinase), PLC (Phospholipase C), PLD (Phospholipase D), Raf and WASP (Wiskott-Aldrich syndrome protein). As a key modulator of the immune system, complement derived proteins clearly have the capacity to a
Ls. Activation of effector T-cells and secretion of cytokines define a key development in course of disease associated with dengue virus infection. Four patient studies done in Vietnam[28], India[29], Cuba[30], and Brazil[31] all showed increases in INF, TNF, IL-10, IL-1, IL-6, IL-8, and MCP1 amongst a variety of other cytokines. In vitro studies, IFN, IL-6, TNF, and RANTES upregulation also have
Ivation is greatly enhanced. When they added purified NS1 protein to normal or convalescent sera they found synonymous results with NS1 activating complement and complement activation being synergized by anti-dengue antibodies. While NS1 could clearly activate complement in the fluid phase it was unable activate complement when stably expressed on the surface of cells. However, when patient sampl
Er positive cells were stained with Ki67, they show definitive proliferation. The cells are also found to be 'massively' apoptotic as determined by TUNEL staining. The balance of apoptotic cells with proliferative cells may skew T cell responses toward a crossreactive phenotype. When looking at the specific T-cells involved in secondary infections with DENV1, many of the T-cells show a preference
Reactive antibodies activate complement still further. The increase in alternative complement proteins, complement receptors and C protein all facilitate a positive feedback loop that can have dangerous consequences in a dengue infected patient.ConclusionThree immune components interact to produce a confluence of symptoms that define DHF/DSS. Dengue virus initially infects immature dendritic cell
Helial cells, smooth muscles cells, and activated T-cells, but, interestingly, not na e T-cells. C5aR also activates a number of downstream signaling pathways including PI3K- (Phosophoinosital -3 Kinase), PLC (Phospholipase C), PLD (Phospholipase D), Raf and WASP (Wiskott-Aldrich syndrome protein). As a key modulator of the immune system, complement derived proteins clearly have the capacity to a


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