Dengue

Dengue is caused by infection with dengue virus (DENV), a positive-stranded enveloped RNA flavivirus with four antigenically distinct serotypes, DENV-1 to DENV-4. Transmission is principally by Aedes mosquitoes, especially Aedes aegypti, with Aedes albopictus also recognized as a competent vector. The literature also notes that heterotypic infection with different serotypes is associated with more severe disease.

Disease pathogenesis reflects interactions between the virus, host genes, and the host immune response. Antibody-dependent enhancement, memory cross-reactive T cells, anti-DENV NS1 antibodies, and autoimmunity are described as major contributors, with Fcγ receptor-mediated enhancement promoting cytokine release, endothelial dysfunction, and increased vascular permeability. Severe dengue is associated with thrombocytopenia, leucopenia, and vascular leak.

Infection with a different dengue serotype after prior exposure is a major risk factor for more severe disease. Host genetic factors and immune factors such as antibody-dependent enhancement, cross-reactive T-cell responses, and anti-NS1 antibodies are also implicated. Exposure risk is increased in areas where competent Aedes vectors are established, including tropical and subtropical regions and newly infested temperate regions.

The supplied grounding does not describe specific treatment modalities or drug classes for dengue. It supports vector control and enhanced surveillance as public-health measures to reduce transmission. No therapeutic standard of care is supported here.