title: Caraparu virus induces damage and alterations in antioxidant defenses in the liver of BALB/c mice after subcutaneous infection.
abstract: Oxidative stress is a disturbance in the oxidant-antioxidant 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-α (TNF-α) 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.
authors.affiliation: Núcleo de Pesquisas em Ciências Biológicas, NUPEB, Universidade Federal de Ouro Preto, Ouro Preto, Minas Gerais, Brazil.
authors.forename: Fernanda Caetano
authors.initials: FC
authors.lastname: Camini
authors.forename: Letícia Trindade
authors.initials: LT
authors.lastname: Almeida
authors.forename: Carolina Silva
authors.initials: CS
authors.lastname: Bernardes
authors.forename: Maísa
authors.initials: M
authors.lastname: Silva
authors.forename: Maria Lúcia
authors.initials: ML
authors.lastname: Pedrosa
authors.forename: Daniela Caldeira
authors.initials: DC
authors.lastname: Costa
authors.forename: Wanderson Geraldo
authors.initials: WG
authors.lastname: de Lima
authors.forename: Carla
authors.initials: C
authors.lastname: do Amaral Pinto
authors.forename: Paulo César Peregrino
authors.initials: PC
authors.lastname: Ferreira
authors.forename: José Carlos
authors.initials: JC
authors.lastname: de Magalhães
authors.forename: Cintia Lopes
authors.initials: CL
authors.lastname: de Brito Magalhães
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002044:Bunyaviridae Infections / Q000473:pathology*; D005978:Glutathione / Q000096:biosynthesis; D006505:Hepatitis / Q000821:virology; D008099:Liver / Q000473:pathology* / Q000821:virology; D051379:Mice; D008807:Mice, Inbred BALB C; D016851:Orthobunyavirus / Q000145:classification / Q000472:pathogenicity*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D014779:Virus Replication
chemical_list: D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005978:Glutathione