Abstract
BackgroundSelenium (Se) deficiency plays an important role in viral pathogenesis. To understand the effects of Se deficiency on West Nile virus (WNV) infection, we analyzed cytopathogenicity, apoptosis and viral replication kinetics, using a newly developed Se-deficient cell culture system.ResultsBoth Vero and SK-N-SH cells grown in Se-deficient media exhibited a gradual loss of glutathione peroxidase (GPx1) activity without any significant effect on cell growth and viability. In SK-N-SH cells, Se deficiency had no effect on the expression of key antioxidant enzymes, including manganese- and copper-zinc superoxide dismutase (MnSOD and CuZnSOD), catalase and inducible nitric oxide synthase, whereas Vero cells demonstrated a significant increase in the expression of MnSOD and an overall increase in oxidative stress (OS) at day 7 post-induction of Se deficiency. At 2 days after infection with WNV, CPE and cell death were significantly higher in WNV-infected Se-deficient Vero cells, compared to WNV-infected control cells. Furthermore, WNV-induced apoptosis was significantly heightened in Se-deficient cells and was contributed by loss of mitochondrial membrane potential and increased caspase activity. However, no significant difference was found in WNV copy numbers between control, Se-adequate and Se-deficient cell cultures.ConclusionOverall results demonstrate that the in vitro Se-deficient model can be used to study responses of WNV to this essential nutrient. Although Se deficiency has no in vitro effect on WNV replication kinetics, adequate Se is presumably critical to protect WNV-infected cells against virus-induced cell death.
Highlights
IntroductionTo understand the effects of Se deficiency on West Nile virus (WNV) infection, we analyzed cytopathogenicity, apoptosis and viral replication kinetics, using a newly developed Se-deficient cell culture system
Selenium (Se) deficiency plays an important role in viral pathogenesis
Effect of Se deficiency on Vero and SK-N-SH cells fetal bovine serum (FBS) is the main source of Se for cells grown in vitro
Summary
To understand the effects of Se deficiency on West Nile virus (WNV) infection, we analyzed cytopathogenicity, apoptosis and viral replication kinetics, using a newly developed Se-deficient cell culture system. As such, impaired antioxidative and immune responses associated with inadequate dietary Se results in increased disease severity following infections with HIV, influenza virus and Coxsackie virus [2,3]. In HIV- infected patients, low plasma Se levels are associated with the development of severe cardiomyopathy [4,5]. Point mutations in Coxsackie virus B3 (CVB3/0) and influenza A virus (H3N2) have been associated with increased disease severity in Se-deficient mice [7,8,9], and an increase in reactive oxygen species (ROS) was demonstrated to enhance HIV replication in Tlymphocytic and monocytic cells [10,11,12]. Se deficiency leads to increased virulence and evolution of viral quasispecies [13,14]
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