Please use this identifier to cite or link to this item:
Title: Caraparu virus induces damage and alterations in antioxidant defenses in the liver of BALB/c mice after subcutaneous infection.
Authors: Camini, Fernanda Caetano
Almeida, Letícia Trindade
Bernardes, Carolina Silva
Silva, Maísa
Pedrosa, Maria Lúcia
Costa, Daniela Caldeira
Lima, Wanderson Geraldo de
Pinto, Carla do Amaral
Ferreira, Paulo César Peregrino
Magalhães, José Carlos de
Magalhães, Cíntia Lopes de Brito
Issue Date: 2014
Citation: CAMINI, F. C. et al. Caraparu virus induces damage and alterations in antioxidant defenses in the liver of BALB/c mice after subcutaneous infection. Archives of Virology, v. 159, p. 2621-2632, 2014. Disponível em: <>. Acesso em: 19 fev. 2017.
Abstract: Oxidative stress is a disturbance in the oxidantantioxidant balance leading to potential cellular damage. Most cells can tolerate a mild degree of oxidative stress because they have a system that counteracts oxidation that includes antioxidant molecules such as glutathione (GSH) and superoxide dismutase (SOD). Disruption of the host antioxidant status has been recognized as an important contributor to the pathogenesis of many viruses. Caraparu virus (CARV) is a member of group C of the Bunyaviridae family of viruses. In South American countries, group C bunyaviruses are among the common agents of human febrile illness and have caused multiple notable outbreaks of human disease in recent decades; nevertheless, little is known about the pathogenic characteristics of these viruses. The purpose of this study was to examine the hepatic pathogenesis of CARV in mice and the involvement of oxidative stress and antioxidant defenses on this pathology. Following subcutaneous infection of BALB/c mice, CARV was detected in the liver, and histopathology revealed acute hepatitis. Increased serum levels of aspartate and alanine aminotransferases (AST/ALT) and greater hepatic expression of the proinflammatory cytokine tumor necrosis factor- a (TNF-a) were found in infected animals. CARV infection did not alter the biomarkers of oxidative stress but caused an increase in GSH content and altered the expression and activity of SOD. This is the first report of an alteration of oxidative homeostasis upon CARV infection, which may, in part, explain the hepatic pathogenesis of this virus, as well as the pathogenesis of other Bunyaviridae members.
ISSN: 1432-8798
Appears in Collections:DECBI - Artigos publicados em periódicos

Files in This Item:
File Description SizeFormat 
  Restricted Access
1,17 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.