RESUMO
Yellow fever (YF) is an infectious disease considered a public health problem in tropical and subtropical areas. YF has many pathophysiological events that are correlated with the host immune response. In this study, the in situ Th22 cytokine profile was evaluated. Liver tissue samples were collected from 21 YFV-positive patients who died of the disease and five flavivirus-negative controls who died of other causes and whose hepatic parenchyma architecture was preserved. Immunohistochemical (IHC) analysis of tissues in the hepatic parenchyma of YF cases showed significantly higher expression of interleukin (IL)-22, IL-13, tumour necrosis factor-alpha, and FGF basic (FGF b) in YFV-positive cases than that in flavivirus-negative controls. These results indicate that the response of Th22 cytokines emerges as an alternative for a better understanding of adaptive immunity in the hepatic parenchyma, highlighting the role of cytokines in the repair and suppressive responses in the immunopathogenesis of YFV infection.
Assuntos
Doenças Transmissíveis , Flavivirus , Hepatopatias , Febre Amarela , Citocinas , Humanos , Febre Amarela/patologia , Vírus da Febre AmarelaRESUMO
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.
Assuntos
Epidemias , Hepatite A , Hepatite , Febre Amarela , Apoptose , Hepatite A/epidemiologia , Humanos , Vírus da Febre AmarelaRESUMO
Tacaiuma virus (TCMV) is antigenically characterized as a member of the Anopheles A complex in the Orthobunyavirus genus, Peribunyaviridae family (Bunyavirales order). Clinically, the TCMV infection is characterized by acute febrile illness with myalgia and arthralgia lasting three to five days. However, the genomic and evolutionary aspect of this virus has not been elucidated. In this study, we described the complete coding sequences of three segments of two TCMV strains isolated in Brazil and three complete coding sequences of the small segment of three TCMV strains. All the strains sequenced in this study showed the typical genomic organization of orthobunyaviruses that infect vertebrates, except for the absence of the open reading frame that encodes the well-described non-structural small protein. This study presents the genomic and evolutionary characterization of TCMV strains and would be helpful for diagnostic purposes and epidemiology.