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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
Ntegrin) (CD209) on dendritic cells [17-19]. Dendritic cells are considered crucial to fighting viral infections because of their ability to acquire and display viral antigens that would otherwisePage 2 of(page number not for citation purposes)Virology Journal 2009, 6:http://www.virologyj.com/content/6/1/evade the immune system. Dendritic cells affect the dengue virus in two ways. Immature dendri
Risk. Mild dengue fever presents with headache, fever, rash, myalgia, osteogenic pain, and lethargy. Severe disease can manifest as dengue shock syndrome (DSS) or dengue hemorrhagic fever (DHF). Symptoms of DSS/DHF are leukopenia, low blood volume and pressure encephalitis, cold and sweaty skin, gastrointestinal bleeding, and spontaneous bleeding from gums and nose. Currently, there are no therap
Cquire the disease the first time (primary infections) are often asymptomatic and will generate immunity to homologous strains of the virus; however, ninety percent of DHF/ DSS cases come from a second exposure (secondary infection) to a heterologus strain of dengue[5]. Patients with a secondary heterotypic infection are at least 40-80 times more likely to develop DHF/DSS as patients with a prima
Nce in Hawaii, Cuba, and Thailand[9] shows populations with previous exposure to the dengue virus are at an increased risk for DHF/DSS. Also infants born to dengue immune mothers were shown to be at an increased risk for DHF/DSS[10]. It's not clear how antibodies enhance viral infection. Onehypothesis suggests that non-neutralizing antibodies direct active virions to permissive cells in the immun
Nce in Hawaii, Cuba, and Thailand[9] shows populations with previous exposure to the dengue virus are at an increased risk for DHF/DSS. Also infants born to dengue immune mothers were shown to be at an increased risk for DHF/DSS[10]. It's not clear how antibodies enhance viral infection. Onehypothesis suggests that non-neutralizing antibodies direct active virions to permissive cells in the immun
Ntegrin) (CD209) on dendritic cells [17-19]. Dendritic cells are considered crucial to fighting viral infections because of their ability to acquire and display viral antigens that would otherwisePage 2 of(page number not for citation purposes)Virology Journal 2009, 6:http://www.virologyj.com/content/6/1/evade the immune system. Dendritic cells affect the dengue virus in two ways. Immature dendri
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
Ic cells have been shown to attenuate the immune response and promote tolerance in a way analogous to Tregulatory cells. DCs can also activate B-cells through costimulation of CD40, IL-6, and IL-12. The crux of DC interaction is in two places: DC maturation and T-cell synapse. Either point represents a potential target for dengue virus immune evasion. Should DCs fail to mature properly, they will
Nce in Hawaii, Cuba, and Thailand[9] shows populations with previous exposure to the dengue virus are at an increased risk for DHF/DSS. Also infants born to dengue immune mothers were shown to be at an increased risk for DHF/DSS[10]. It's not clear how antibodies enhance viral infection. Onehypothesis suggests that non-neutralizing antibodies direct active virions to permissive cells in the immun
Cquire the disease the first time (primary infections) are often asymptomatic and will generate immunity to homologous strains of the virus; however, ninety percent of DHF/ DSS cases come from a second exposure (secondary infection) to a heterologus strain of dengue[5]. Patients with a secondary heterotypic infection are at least 40-80 times more likely to develop DHF/DSS as patients with a prima
Nce in Hawaii, Cuba, and Thailand[9] shows populations with previous exposure to the dengue virus are at an increased risk for DHF/DSS. Also infants born to dengue immune mothers were shown to be at an increased risk for DHF/DSS[10]. It's not clear how antibodies enhance viral infection. Onehypothesis suggests that non-neutralizing antibodies direct active virions to permissive cells in the immun
At typically binds to IgG and is composed of an chain for domain recognition, an ITAM (immunoreceptor tyrosine based activation motif), and a chain that is responsible for signal transduction. It is thought that IgM does not play a direct role in ADE and instead contributes to disease pathogenesis through activation of complement receptors[13]. IgM antibody enhancement was abrogated when C3R is
Ells can increase viral RNA production by over 100-fold making dendritic cells potent components in dengue pathogenesis[20]. Infected dendritic cells also contribute to vascular leak through the production of matrix metalloproteinases (MMPs). MMP-2, MMP-13, and MMP-9 were all dramatically increased in immature dendritic cells infected with DENV2. As a result cell-cell adhesion in cells co-culture


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