Infection with dengue virus (DENV) causes both mild
dengue fever and
severe dengue diseases, such as
dengue hemorrhagic fever and
dengue shock syndrome. The pathogenic mechanisms for DENV are complicated, involving viral cytotoxicity, immunopathogenesis, autoimmunity, and underlying host diseases. Viral load correlates with disease severity, while the antibody-dependent enhancement of
infection largely determines the secondary effects of DENV
infection. Epidemiological and experimental studies have revealed an association between the plasma levels of
interleukin (IL)-10, which is the master anti-inflammatory
cytokine, and disease severity in patients with DENV
infection. Based on current knowledge of IL-10-mediated immune regulation during
infection, researchers speculate an emerging role for
IL-10 in clinical disease prognosis and
dengue pathogenesis. However, the regulation of
dengue pathogenesis has not been fully elucidated. This review article discusses the regulation and implications of
IL-10 in DENV
infection. For future strategies against DENV
infection, manipulating
IL-10 may be an effective
antiviral treatment in addition to the development of a safe
dengue vaccine.