Avaliação do dano hepático causado por flaviviroses associadas ou não à diabetes mellitus

Abstract

Flaviviruses pose a significant challenge to global health, as they have the ability to infect arthropods and cause various damages to the human body. Among them, the arbovirus known as Zika (ZIKV) was discovered in 1947 in Africa, had its first confirmed case in Brazil, it was introduced in 2015, and due to the large number of existing vectors, it quickly dissipated. ZIKV has been studied in a more relevant way since it was identified as a cause of microcephaly and other neurological processes in newborns. Furthermore, liver damage has also been reported in association with the infection and Other flaviviruses studied in this research, as dengue and yellow fever. Studies show cell loss caused by cytotoxicity due to viral infection in hepatocytes after infection with ZIKV, which is also observed in viral hepatitis. In acute viral infections, individuals with pre-existing chronic diseases, such as diabetes mellitus, are more likely to develop more serious conditions. Diabetes also plays an important role in the initiation and progression of liver damage. Therefore, this study evaluated the effects of the association of diabetes mellitus and ZIKV infection on the liver parenchyma of male BALB/c mice in na experimental research and the hepatic damage caused by flaviviruses in a sistematic review. Diabetes was induced with streptozotocin diluted in sodium citrate buffer. Infection was performed after immunosuppression with dexamethasone and the virus was inoculated intraperitoneally in RPMI medium. The vehicles used for dilution were administered to controls to simulate stress. In 28 days, the animals in each group were euthanized. The liver was collected, weighed and processed for morphometry, histopathology, oxidative stress and liver damage analysis. Changes were found in the activities of the antioxidant enzymes CAT in the Zika group, carbonyl protein and FRAP in the Zika, diabetic and diabetic groups with Zika, elevation of ALT and AST in the diabetic and diabetic groups with Zika, elevation of glycemia, lactate levels, in addition to morphological changes with cell death and hydropic degeneration in all groups. Therefore, diabetes prolongs the activity of Zika viremia and that there is a negative impact on liver functionality caused by the Zika virus and diabetes.