Development of a convenient immunochromatographic strip for the diagnosis of infection with Japanese encephalitis virus in swine

Li, Yaoming; Hou, Lihua; Ye, Jing; Liu, Xueqin; Dan, Hanbing; Jin, Meilin; Chen, Huanchun; Cao, Shengbo

doi:10.1016/j.jviromet.2010.04.015

Cited by 46 publications

(42 citation statements)

References 19 publications

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“…A 10% (wt/vol) suspension was prepared by homogenizing the brain in Dulbecco modified Eagle medium (DMEM). The homogenate was centrifuged to remove debris, and the supernatant was collected and stored at Ϫ80°C (26). A baby hamster kidney fibroblast cell line (BHK-21) was used for viral titration.…”

Section: Methodsmentioning

confidence: 99%

Viral Infection of the Central Nervous System and Neuroinflammation Precede Blood-Brain Barrier Disruption during Japanese Encephalitis Virus Infection

Wang

Lan

et al. 2015

J Virol

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204

218

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Japanese encephalitis is an acute zoonotic, mosquito-borne disease caused by Japanese encephalitis virus (JEV). Japanese encephalitis is characterized by extensive inflammation in the central nervous system (CNS) and disruption of the blood-brain barrier (BBB). However, the pathogenic mechanisms contributing to the BBB disruption are not known. Here, using a mouse model of intravenous JEV infection, we show that virus titers increased exponentially in the brain from 2 to 5 days postinfection. This was accompanied by an early, dramatic increase in the level of inflammatory cytokines and chemokines in the brain. Enhancement of BBB permeability, however, was not observed until day 4, suggesting that viral entry and the onset of inflammation in the CNS occurred prior to BBB damage. In vitro studies revealed that direct infection with JEV could not induce changes in the permeability of brain microvascular endothelial cell monolayers. However, brain extracts derived from symptomatic JEV-infected mice, but not from mock-infected mice, induced significant permeability of the endothelial monolayer. Consistent with a role for inflammatory mediators in BBB disruption, the administration of gamma interferon-neutralizing antibody ameliorated the enhancement of BBB permeability in JEV-infected mice. Taken together, our data suggest that JEV enters the CNS, propagates in neurons, and induces the production of inflammatory cytokines and chemokines, which result in the disruption of the BBB. IMPORTANCEJapanese encephalitis (JE) is the leading cause of viral encephalitis in Asia, resulting in 70,000 cases each year, in which approximately 20 to 30% of cases are fatal, and a high proportion of patients survive with serious neurological and psychiatric sequelae. Pathologically, JEV infection causes an acute encephalopathy accompanied by BBB dysfunction; however, the mechanism is not clear. Thus, understanding the mechanisms of BBB disruption in JEV infection is important. Our data demonstrate that JEV gains entry into the CNS prior to BBB disruption. Furthermore, it is not JEV infection per se, but the inflammatory cytokines/ chemokines induced by JEV infection that inhibit the expression of TJ proteins and ultimately result in the enhancement of BBB permeability. Neutralization of gamma interferon (IFN-␥) ameliorated the enhancement of BBB permeability in JEV-infected mice, suggesting that IFN-␥ could be a potential therapeutic target. This study would lead to identification of potential therapeutic avenues for the treatment of JEV infection. J apanese encephalitis (JE) is an acute zoonotic, mosquito-borne infectious disease caused by JE virus (JEV) infection. JEV is a single-stranded, positive-sense RNA virus, belonging to the genus Flavivirus of the family Flaviviridae (1, 2). JEV is a neurotropic virus and infection causes an acute encephalopathy. JE commonly affects children in the South Pacific regions of Asia (3, 4). Of nearly 70,000 cases of JE reported each year, ca. 20 to 30% of cases are fatal, and a high proport...

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Section: Methodsmentioning

confidence: 99%

Viral Infection of the Central Nervous System and Neuroinflammation Precede Blood-Brain Barrier Disruption during Japanese Encephalitis Virus Infection

Wang

Lan

et al. 2015

J Virol

Self Cite

204

218

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“…Here, three differential centrifugations were performed during the purification of the virus particles to reduce contamination and false-positive results. The antibody couples with gold sol more effectively when the pH is a little higher than the isoelectric point (pI) of the labeling antibody (the pI of IgY is 5.2) (Li et al, 2010). In this study, a titration was performed to determine the optimum pH of the colloidal gold solution.…”

Section: Discussionmentioning

confidence: 99%

Development of a colloidal gold immunochromatographic strip for the rapid detection of soft-shelled turtle systemic septicemia spherical virus

Zhang

Liu

et al. 2015

Journal of Virological Methods

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“…Monoclonal antibodies (MAbs) that recognized prM were kindly provided by R. H. Hua (HarBin Veterinary Research Institute, Harbin, China). E protein linear epitope (LE) MAb (1:200) was generated in our laboratory (Li et al, 2010). The E protein conformational epitope (CE) MAb (1:10) was purchased from Thermo Scientific (USA).…”

Section: Methodsmentioning

confidence: 99%

N-glycosylation of the premembrane protein of Japanese encephalitis virus is critical for folding of the envelope protein and assembly of virus-like particles

J¹,

Mei²,

Wang³

et al. 2013

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Summary. -Premembrane (prM) and envelope (E) proteins, the major structural proteins of Japanese encephalitis virus (JEV) each contain single potential N-glycosylation site. In this study, the role of N-glycosylation of these proteins on their folding and activity were investigated. Three mutant prM and/or E (prM-E) genes lacking N-glycosylation sites were generated by site-directed mutagenesis. The effects of the N-glycan on folding, secretion and cytotoxicity of mutant proteins were determined by comparison with their wild type (wt) counterparts. Removal of N-glycan from the prM protein resulted in a complete misfolding of the E protein and failure to form virus-like particles (VLPs). A similar removal of N-glycan from the E protein led to a low efficiency of its folding and VLPs formation. The secretion and cytotoxicity of the E protein was also markedly impaired in case the glycosylation sites in the prM or E or both proteins were removed. These results suggest that the N-glycosylation of the prM protein is critical to the folding of the E protein, which makes it pivotal in the cytotoxicity of JEV particles and their production.Keywords: Japanese encephalitis virus; premembrane protein; envelope protein; N-glycosylation; protein folding; virus-like particles; secretion; cytotoxicity * Corresponding author. E-mail: syf@mail.hzau.edu.cn; phone: +86-27-87618028. Abbreviations: CE = conformational epitope; E = envelope; ER = endocytoplasmic reticulum; JEV = Japanese encephalitis virus; LE = linear epitope; MAb(s) = monoclonal antibody(ies) prM = premembrane; VLPs = virus-like particles

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Development of a convenient immunochromatographic strip for the diagnosis of infection with Japanese encephalitis virus in swine

Cited by 46 publications

References 19 publications

Viral Infection of the Central Nervous System and Neuroinflammation Precede Blood-Brain Barrier Disruption during Japanese Encephalitis Virus Infection

Viral Infection of the Central Nervous System and Neuroinflammation Precede Blood-Brain Barrier Disruption during Japanese Encephalitis Virus Infection

Development of a colloidal gold immunochromatographic strip for the rapid detection of soft-shelled turtle systemic septicemia spherical virus

N-glycosylation of the premembrane protein of Japanese encephalitis virus is critical for folding of the envelope protein and assembly of virus-like particles

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