D — Dengue Virus
Dengue virus (DENV) is a mosquito-borne flavivirus with four antigenically distinct serotypes (DENV-1 to -4). It is an enveloped, positive-sense RNA virus that replicates in the cytoplasm using a single polyprotein cleaved into structural and nonstructural proteins.
Following inoculation by Aedes mosquitoes, dengue infects dendritic cells and monocytes via receptors including DC-SIGN. A hallmark of dengue pathogenesis is antibody-dependent enhancement (ADE). During secondary infection with a different serotype, non-neutralizing antibodies facilitate viral entry into Fcγ receptor–bearing cells, increasing viral replication.
Severe dengue involves vascular permeability, plasma leakage, thrombocytopenia, and shock. NS1 protein contributes to endothelial dysfunction and complement activation. Disease severity reflects both viral factors and host immune responses, including cytokine storms and cross-reactive T-cell activation.
Clinically, dengue ranges from self-limited febrile illness to severe dengue hemorrhagic fever and shock syndrome. Research challenges include vaccine development that avoids ADE, antiviral discovery, and understanding immune correlates of protection versus pathogenesis.
Dengue virus (DENV) is a mosquito-borne flavivirus with four antigenically distinct serotypes (DENV-1 to -4). It is an enveloped, positive-sense RNA virus that replicates in the cytoplasm using a single polyprotein cleaved into structural and nonstructural proteins.
Following inoculation by Aedes mosquitoes, dengue infects dendritic cells and monocytes via receptors including DC-SIGN. A hallmark of dengue pathogenesis is antibody-dependent enhancement (ADE). During secondary infection with a different serotype, non-neutralizing antibodies facilitate viral entry into Fcγ receptor–bearing cells, increasing viral replication.
Severe dengue involves vascular permeability, plasma leakage, thrombocytopenia, and shock. NS1 protein contributes to endothelial dysfunction and complement activation. Disease severity reflects both viral factors and host immune responses, including cytokine storms and cross-reactive T-cell activation.
Clinically, dengue ranges from self-limited febrile illness to severe dengue hemorrhagic fever and shock syndrome. Research challenges include vaccine development that avoids ADE, antiviral discovery, and understanding immune correlates of protection versus pathogenesis.