Caraparu virus induces damage and alterations in antioxidant defenses in the liver of BALB/c mice after subcutaneous infection.
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2014
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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.
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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: <http://link.springer.com/article/10.1007%2Fs00705-014-2123-2>. Acesso em: 19 fev. 2017.