LAUSR

Dengue is a mosquito-borne infection caused by dengue virus (DENV) of the Flaviviridae family. There are four distinct serotypes, DENV-1,-2,-3,-4, which cause outbreaks globally. Infection is often self-resolving, and lifelong immunity against the infecting serotype can be achieved after exposure. However, in some individuals, homologous infection may still result in symptomatic dengue [1]. There is usually limited protection against heterotypic infections by three other DENV serotypes, as cross-protection is short-lived [2]. After this window of “protection”, subsequent infection with a different serotype may increase the risk of develop-ing severe dengue [3,4]. Antibody-dependent enhancement (ADE) in dengue, a process mainly mediated by immunoglobulin G (IgG), is believed to be one of the major underlying mechanisms leading to increased severity in secondary DENV infection. ADE was shown to enhance viral entry into immune cells via their Fc γ receptors (Fc γ R), which promotes viral replication, leading to increased viremia and pro-inflammatory responses. These contribute to disease pathologies including vascular hyperpermeability, a common cause