Factors involved in the apoptotic cell death mechanism in yellow fever hepatitis

• Autor(a) principal: Lopes, Jeferson da Costa
• Data de Publicação: 2022
• Outros Autores: Falcão, Luiz Fábio Magno, Martins Filho, Arnaldo Jorge, Carvalho, Marcos Luiz Gaia, Mendes, Caio Cesar Henriques, Olímpio, Fábio Alves, Miranda, Vanessa do Socorro Cabral, Santos, Lais Carneiro dos, Chiang, Jannifer Oliveira, Cruz, Ana Cecília Ribeiro, Galúcio, Vanessa Costa Alves, Azevedo, Raimunda do Socorro da Silva, Martins, Lívia Caricio, Duarte, Maria Irma Seixas, Sousa, Jorge Rodrigues de, Vasconcelos, Pedro Fernando da Costa, Quaresma, Juarez Antônio Simões
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Digital do Instituto Evandro Chagas (Patuá)
• Texto Completo: https://patua.iec.gov.br/handle/iec/4577
• topic: Febre Amarela / patologia; Apoptose; Proteínas Reguladoras de Apoptose; Hepatite / patologia; Morte Celular / imunologia

Yellow fever (YF), a non-contagious infectious disease, is endemic or enzootic to the tropical regions of the Americas and Africa. Periodic outbreaks or epidemics have a significant impact on public health. Programmed cell death, or apoptosis, is generally characterised by distinct morphological changes and energy-dependent biochemical pathways. In this study, we performed immunohistochemistry analysis to identify and quantify proteases and protein targets involved in the cascade that triggers apoptosis in YF virus (YFV)-infected human hepatocytes. Liver tissue samples were collected from 26 individuals, among whom 21 were diagnosed as YF-positive, and five were flavivirus-negative and died due to other causes. The histopathological alterations in YFV-positive cases were characterised by the presence of apoptotic bodies, steatosis, cellular swelling, and extensive necrosis and haemorrhage in the hepatic lobules. Additionally, we observed an abundance of inflammatory infiltrates in the portal tract. The expression of various apoptotic markers in the hepatic parenchyma, including CASPASE 3, CASPASE 8, BAX, FAS, FASL, GRANZYME B, and SURVIVIN, differed between YFV-positive cases and controls. Collectively, this study confirmed the complexity of YFV infection-induced apoptosis in situ. However, our data suggest that apoptosis in liver parenchyma lesions may significantly contribute to the pathogenesis of fatal YF in humans.