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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 immune
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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 immune
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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-cultured
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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
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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 immune
1
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 immune
1
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 dendrit
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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 dendrit
1
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
1
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 immune