Immunologic Crosstalk\nand Host-Specific Immune Signature\nAssociated with Dengue

In tropical and subtropical regions, dengue fever is\na common febrile\nillness that is mostly spread by Aedes mosquitoes. Urban population\nmigration, inadequate water storage facilities, and high mosquito\ndensity are features associated with this disease. The severity of\nthe illness ranges from mild to deadly dengue hemorrhagic fever (DHF)\nand dengue shock syndrome (DSS), often with severe cases causing profound\nshock from extensive plasma leakage, and may result in demise. The\nsymptoms of the illness include headache, myalgia, retro-orbital pain,\nand hemorrhagic signs. There may also be an intermittent shift in\nblood vessel integrity and coagulation, but recovery is typically\ncomplete and rapid. In this review, we emphasize the immunological\naspects of this illness. The intricate interactions among the virus,\nhost genes, and host immune systems impact the pathophysiology of\ndengue. Postinfection antibody-dependent enhancement is prominent,\nwhich significantly influences the etiology and virulence of the disease.\nWhereas the severe form only manifests when the host immune system\nis actively working to eradicate the infection by secreting several\ninflammatory cytokines, chemokines, and lipid mediators, for example,\nearly dengue virus infection (DVI) resulted in the production of Interleukin\n2 (IL-2), IL-6, and later infection, IL-4, IL-5, and IL-10. Higher\nconcentrations of interferons gamma (IFN-gamma), granulocyte-macrophage\ncolony-stimulating factor (GM-CSF), macrophage migration inhibitory\nfactor (MIF), IL-1, IL-2, IL-4, IL-6, IL-7, IL-10, IL-12, and IL-13\nwere found in DHF patients. These are significantly more prevalent\nin severe infections than in mild ones. Numerous immunopathogenic\nprocesses involving both virus and host variables influence the severity\nof dengue. There is growing evidence that a compromised immune system\nlimits viral clearance and causes severe inflammation, which in turn\ncauses dengue hemorrhagic fever and dengue shock syndrome. Furthermore,\nthe capacity of DENV to infect a broad range of immune cells, such\nas macrophages, dendritic cells, mast cells, T and B cells, and monocytes,\nfurther dysregulates these cells’ antiviral activities, leading\nto the spread of the virus. Even though a number of risk factors linked\nto the advancement of the disease have been suggested, further research\nand evaluation of novel technologies are necessary to understand the\ncomplicated etiology and develop reliable and effective vaccines to\nfight against this febrile illness.