Camini Fernanda Caetano, Almeida Letícia Trindade, Bernardes Carolina Silva, Silva Maísa, Pedrosa Maria Lúcia, Costa Daniela Caldeira, de Lima Wanderson Geraldo, do Amaral Pinto Carla, Ferreira Paulo César Peregrino, de Magalhães José Carlos, de Brito Magalhães Cintia Lopes
Núcleo de Pesquisas em Ciências Biológicas, NUPEB, Universidade Federal de Ouro Preto, Ouro Preto, Minas Gerais, Brazil.
Arch Virol. 2014 Oct;159(10):2621-32. doi: 10.1007/s00705-014-2123-2. Epub 2014 May 27.
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.
氧化应激是氧化剂-抗氧化剂平衡的紊乱，会导致潜在的细胞损伤。大多数细胞能够耐受轻度的氧化应激，因为它们拥有一个对抗氧化的系统，该系统包括抗氧化分子，如谷胱甘肽（GSH）和超氧化物歧化酶（SOD）。宿主抗氧化状态的破坏已被认为是许多病毒发病机制的重要因素。卡拉帕鲁病毒（CARV）是布尼亚病毒科C组病毒的成员。在南美国家，C组布尼亚病毒是人类发热性疾病的常见病原体之一，近几十年来已引发多起引人注目的人类疾病疫情；然而，对这些病毒的致病特征知之甚少。本研究的目的是研究CARV在小鼠中的肝脏发病机制以及氧化应激和抗氧化防御在该病理过程中的作用。BALB/c小鼠皮下感染后，在肝脏中检测到CARV，组织病理学显示为急性肝炎。在感染动物中发现血清天冬氨酸和丙氨酸转氨酶（AST/ALT）水平升高，促炎细胞因子肿瘤坏死因子-α（TNF-α）的肝脏表达增加。CARV感染并未改变氧化应激的生物标志物，但导致GSH含量增加，并改变了SOD的表达和活性。这是关于CARV感染后氧化稳态改变的首次报道，这可能部分解释了该病毒的肝脏发病机制以及其他布尼亚病毒科成员的发病机制。
