Autor(es): Holanda, Gustavo Moraes ; Casseb, Samir Mansour Moraes ; Quaresma, Juarez Antonio Sim?es ; Vasconcelos, Pedro Fernando da Costa ; cruz, Ana Cec?lia Ribeiro
Data: 2019
Origem: Oasisbr
Assunto(s): Febre Amarela / virologia; F?gado / patologia; F?gado / les?es; Macr?fagos do F?gado; RNA Mensageiro / gen?tica; Citocinas; Receptores de Citocinas
Minist?rio da Sa?de. Secretaria de Vigil?ncia em Sa?de. Instituto Evandro Chagas. Ananindeua, PA, Brasil.
Minist?rio da Sa?de. Secretaria de Vigil?ncia em Sa?de. Instituto Evandro Chagas. Ananindeua, PA, Brasil.
Minist?rio da Sa?de. Secretaria de Vigil?ncia em Sa?de. Instituto Evandro Chagas. Ananindeua, PA, Brasil.
Minist?rio da Sa?de. Secretaria de Vigil?ncia em Sa?de. Instituto Evandro Chagas. Ananindeua, PA, Brasil.
Minist?rio da Sa?de. Secretaria de Vigil?ncia em Sa?de. Instituto Evandro Chagas. Ananindeua, PA, Brasil.
Yellow fever virus (YFV) penetrates the skin through the bite of a vector mosquito and spreads to various organs, mainly the liver, where it causes lesions and induces necrosis and apoptosis. We evaluated the mRNA expression of various cytokines and the activation of caspases in HepG2 cells infected with YFV. We observed that interferon-? (IFN-?) expression decreased and IFN-?, transforming growth factor (TGF)-? IIIR, interleukin (IL)-6, and IL-8 expression increased in cells infected with genotype 1. In contrast, TNF-? expression increased in cells infected with genotype 2 but not with genotype 1. This provides insights into the role of cytokine regulation in yellow fever.
