Autophagy Mechanism Mediated by the Expression of Beclin 1 in Liver of Fatal Cases of Human Yellow Fever

Yellow fever (YF) infection typically affects the liver, with death primarily attributed to acute hepatic failure. The autophagic process in Flavivirus infection may be a key factor in disease progression. We explored the role of autophagy in the pathogenesis of YF within the liver tissue of fatally affected individuals. Liver samples were collected from 21 Yellow Fever Virus (YFV)-positive patients who died from the disease and five flavivirus-negative controls who died from unrelated causes but had preserved liver parenchymal architecture. The cellular stress environment established in the hepatic parenchyma in fatal virus-positive cases was found to be highly intense. Quantitatively, all markers (iNOS, IL-1β, IL-18, IL-33, BECLIN 1 and RIP3) showed increased expression in relation to the control group, which revealed the involvement of these markers in the pathogenesis of YF. Through correlation tests, we confirmed that both enzymes and proteins collaborate to increase inflammatory activity in the liver parenchyma, mainly in the midzonal zone. These findings suggest that autophagy is associated with the robust inflammatory response in the liver during fatal cases of yellow fever in humans.