Dengue haemorrhagic fever: an evaluation of host innates immune factors in hepatic lesions and their correlation with immunopathogenesis.

Dengue fever challenges public health worldwide. The numerous factors associated with dengue fever severity and mortality risk include host characteristics such as patient age, comorbid conditions, previous dengue virus (DENV) infections, and biochemical biomarkers. Type I IFNs are essential cytokines in orchestrating innate and adaptive immune responses against viral invasion, and their regulation is mediated by IRF-2, which prevents excessive IFN expression. In vitro studies have shown DENV evasion strategies that affect IFN-I production but few have considered the in-situ interrelationship between IFN-I and the virus. This study aims to find elements of innate immunity that induce the anti-viral response and their correlation with the detected alterations in liver lesions. Liver specimens from individuals who died due to dengue were selected according to clinical and laboratory data and serological diagnosis. The specimens were subjected to histological and immunohistochemical evaluation of cells expressing IFN-I, RIG-1, IRF-2, and STING. Viral antigens were detected by an anti-DENV. A high number of cells expressed RIG-1 and IRF-2 when compared to IFN-I and STING. In severe cases of dengue, DENV may play a role in its pathogenesis with properties that induce non-effective immune responses. The virus can evade effective immune responses by impairing the early activation of innate immunity. This immune dysregulation may contribute to the progression of more severe manifestations and seems to play a role in the pathogenesis of hepatic involvement.