Monoclonal Antibodies Against NS3 and NS5 Proteins of Japanese Encephalitis Virus

Chen, Zheng; Shao, Li; Ye, Jing; YongMao, Li; Huang, Shaomei; Chen, Huanchun; Cao, Shengbo

doi:10.1089/hyb.2011.0107

Cited by 17 publications

(11 citation statements)

References 15 publications

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“…Anti-JEV NS3 and NS5 mouse monoclonal antibodies (mAb) were prepared by our laboratory [25]. Commercially available antibodies used include: rabbit anti-Hsp70 polyclonal antibodies (pAbs) (ABclonal), mouse anti-Flag mAb (ABclonal), mouse anti-Myc mAb (Abcam), mouse anti-GAPDH mAb (ABclonal), mouse anti-dsRNA mAb J2 (English & Scientific Consulting Bt.…”

Section: Methodsmentioning

confidence: 99%

Heat Shock Protein 70 Is Associated with Replicase Complex of Japanese Encephalitis Virus and Positively Regulates Viral Genome Replication

Chen

Zhang

et al. 2013

PLoS ONE

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Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes the most prevalent viral encephalitis in Asia. The NS5 protein of JEV is a key component of the viral replicase complex, which plays a crucial role in viral pathogenesis. In this study, tandem affinity purification (TAP) followed by mass spectrometry analysis was performed to identify novel host proteins that interact with NS5. Heat shock protein 70 (Hsp70), eukaryotic elongation factor 1-alpha (eEF-1α) and ras-related nuclear protein (Ran) were demonstrated to interact with NS5. In addition to NS5, Hsp70 was also found to interact with NS3 which is another important member of the replicase complex. It was observed that the cytoplasmic Hsp70 partially colocalizes with the components of viral replicase complex including NS3, NS5 and viral dsRNA during JEV infection. Knockdown of Hsp70 resulted in a significantly reduced JEV genome replication. Further analysis reveals that Hsp70 enhances the stability of viral proteins in JEV replicase complex. These results suggest an important role for Hsp70 in regulating JEV replication, which provides a potential target for the development of anti-JEV therapies.

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Section: Methodsmentioning

confidence: 99%

Heat Shock Protein 70 Is Associated with Replicase Complex of Japanese Encephalitis Virus and Positively Regulates Viral Genome Replication

Chen

Zhang

et al. 2013

PLoS ONE

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“…HRP-conjugated anti-mouse/rabbit secondary Abs (Boster, Wuhan, China) were used. Abs against the NS5 protein of JEV were prepared as previously described (32). Hsa-miR-15b mimics (dsRNA oligonucleotides), inhibitors (single-stranded oligonucleotides chemically modified by 29-Ome), and control oligonucleotides were commercially synthesized by GenePharma (Shanghai, China).…”

Section: Reagentsmentioning

confidence: 99%

MicroRNA-15b Modulates Japanese Encephalitis Virus–Mediated Inflammation via Targeting RNF125

Zhu

Nie

et al. 2015

The Journal of Immunology

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100

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Japanese encephalitis virus (JEV) can target CNS and cause neuroinflammation that is characterized by profound neuronal damage and concomitant microgliosis/astrogliosis. Although microRNAs (miRNAs) have emerged as a major regulatory network with profound effects on inflammatory response, it is less clear how they regulate JEV-induced inflammation. In this study, we found that miR-15b is involved in modulating the JEV-induced inflammatory response. The data demonstrate that miR-15b is upregulated during JEV infection of glial cells and mouse brains. In vitro overexpression of miR-15b enhances the JEV-induced inflammatory response, whereas inhibition of miR-15b decreases it. Mechanistically, ring finger protein 125 (RNF125), a negative regulator of RIG-I signaling, is identified as a direct target of miR-15b in the context of JEV infection. Furthermore, inhibition of RNF125 by miR-15b results in an elevation in RIG-I levels, which, in turn, leads to a higher production of proinflammatory cytokines and type I IFN. In vivo knockdown of virus-induced miR-15b by antagomir-15b restores the expression of RNF125, reduces the production of inflammatory cytokines, attenuates glial activation and neuronal damage, decreases viral burden in the brain, and improves survival in the mouse model. Taken together, our results indicate that miR-15b modulates the inflammatory response during JEV infection by negative regulation of RNF125 expression. Therefore, miR-15b targeting may constitute an interesting and promising approach to control viral-induced neuroinflammation.

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“…The stable hybridoma clones were injected into BALB/c mice intraperitoneally. (12) Subsequently, seroperitoneum was collected from the immunized mice and the MAb was purified by the antibody purification kit according to the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

Monoclonal Antibody Against M Protein of Spring Viremia of Carp Virus

Zhang

Luo

et al. 2015

Monoclonal Antibodies in Immunodiagnosis and Immunotherapy

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Monoclonal Antibodies Against NS3 and NS5 Proteins of Japanese Encephalitis Virus

Cited by 17 publications

References 15 publications

Heat Shock Protein 70 Is Associated with Replicase Complex of Japanese Encephalitis Virus and Positively Regulates Viral Genome Replication

Heat Shock Protein 70 Is Associated with Replicase Complex of Japanese Encephalitis Virus and Positively Regulates Viral Genome Replication

MicroRNA-15b Modulates Japanese Encephalitis Virus–Mediated Inflammation via Targeting RNF125

Monoclonal Antibody Against M Protein of Spring Viremia of Carp Virus

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