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©2013 UpToDate ® Print Email Capillary leak in dengue virus infection Proposed model by which dengue virus (DV) produces a capillary leak syndrome. Monocytes (Mo) are thought to be the primary cellular target for DV. Serotype crossreactive antibodies (Ab), present at the time of second DV infection, bind to virions without neutralization and then enhance the entry of virus into monocytic cells expressing immunoglobulin receptors (FcγR), as show in the left side of the picture. Serotype crossreactive memory T cells, also present at the time of secondary DV infection, recognize viral antigens in the context of class I and II major histocompatibility complex (MHC) molecules. These T cells produce cytokines, such as interferon-gamma (IFNγ) and tumor necrosis factors (TNF) alpha and beta, and lyse DV-infected monocytes. TNF-alpha is also produced in monocytes in response to DV infection and/or interactions with T cells. These cytokines have direct effects on endothelial cells (EC) to induce plasma leakage. Interferon-gamma activates monocytes to increase the expression of MHC molecules and immunoglobulin receptors and the production of TNF-alpha. The complement cascade, activated by virus-antibody complexes and by several cytokines, releases the complement anaphylatoxins C3a and C5a which further increase capillary permeability. Interleukin-2 may contribute by facilitating T cell proliferation.