scholarly journals Long non-coding RNA NONSUST006715.1 suppresses Japanese encephalitis virus proliferation in PK-15 cells

2020 ◽  
Author(s):  
Xiaolong Zhou ◽  
Qiongyu Yuan ◽  
Chen Zhang ◽  
Zhenglie Dai ◽  
Chengtao Du ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Encephalitis Virus ◽  
Host Cells ◽  
Rt Pcr ◽  
Transcription Factor Sp1 ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background: Japanese encephalitis virus is a mosquito-borne neurotropic flavivirus that causes acute viral encephalitis in humans. Pigs are crucial amplifier host of JEV. Recently, increasing evidences have shown that long non-coding RNAs (lncRNAs) play important roles in virus infection. Methods: The JEV proliferation was evaluated after overexpression or knockdown of lncRNA-NONSUST006715.1 using western blotting and reverse-transcription polymerase chain reaction (RT-PCR). C-C chemokine receptor type 1 (CCR1) was found to regulate the expression of lncRNA-NONSUST006715.1 by inhibitors screen. The expression of lncRNA-NONSUST006715.1 was detected using RT-PCR after overexpression or knockdown of transcription factor SP1. In addition, the enrichments of transcription factor SP1 on the promoter of lncRNA-NONSUST006715.1 were analyzed by chromatin immunoprecipitation. Results: In this study, we demonstrated that swine lncRNA-NONSUST006715.1 could suppress JEV proliferation in PK-15 cells. We also found that CCR1 inhibited the expression of lncRNA-NONSUST006715.1 via the transcription factor SP1. In addition, knockdown of CCR1 could upregulated the expression of SP1 and lncRNA-NONSUST006715.1, resulting in resistance to JEV proliferation. Conclusions: These findings illustrate the importance of lncRNAs in virus proliferation, and reveal how this virus regulates lncRNAs in host cells to promote its proliferation.

scholarly journals Inhibition of Japanese encephalitis virus proliferation by long non-coding RNA SUSAJ1 in PK-15 cells

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Xiaolong Zhou ◽  
Qiongyu Yuan ◽  
Chen Zhang ◽  
Zhenglie Dai ◽  
Chengtao Du ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Encephalitis Virus ◽  
Host Cells ◽  
Rt Pcr ◽  
Transcription Factor Sp1 ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background Japanese encephalitis virus is a mosquito-borne neurotropic flavivirus that causes acute viral encephalitis in humans. Pigs are crucial amplifier host of JEV. Recently, increasing evidence has shown that long non-coding RNAs (lncRNAs) play important roles in virus infection. Methods JEV proliferation was evaluated after overexpression or knockdown of lncRNA-SUSAJ1 using western blotting and reverse-transcription polymerase chain reaction (RT-PCR). C–C chemokine receptor type 1 (CCR1) was found to regulate the expression of lncRNA-SUSAJ1 by inhibitors screen. The expression of lncRNA-SUSAJ1 was detected using RT-PCR after overexpression or knockdown of transcription factor SP1. In addition, the enrichments of transcription factor SP1 on the promoter of lncRNA-SUSAJ1 were analyzed by chromatin immunoprecipitation. Results In this study, we demonstrated that swine lncRNA-SUSAJ1 could suppress JEV proliferation in PK-15 cells. We also found that CCR1 inhibited the expression of lncRNA-SUSAJ1 via the transcription factor SP1. In addition, knockdown of CCR1 could upregulated the expression of SP1 and lncRNA-SUSAJ1, resulting in resistance to JEV proliferation. Conclusions These findings illustrate the importance of lncRNAs in virus proliferation, and reveal how this virus regulates lncRNAs in host cells to promote its proliferation.

scholarly journals Long Non-coding RNA NONSUST006715.1 Suppresses Japanese Encephalitis Virus Proliferation in PK-15 Cells

2020 ◽  
Author(s):  
Xiaolong Zhou ◽  
Qiongyu Yuan ◽  
Chen Zhang ◽  
Zhenglie Dai ◽  
Chengtao Du ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Encephalitis Virus ◽  
Host Cells ◽  
Rt Pcr ◽  
Transcription Factor Sp1 ◽  
Non Coding Rna ◽  
Antiviral Function ◽  
Long Non Coding Rna

Abstract Background: Japanese encephalitis virus is a mosquito-borne neurotropic flavivirus that causes acute viral encephalitis in humans. Pigs are crucial amplifier host of JEV. Recently, long non-coding RNAs have received increasing attention for their antiviral function. Methods: LncRNA-NONSUST006715.1 was overexpression or knockdown using western blotting and reverse-transcription polymerase chain reaction (RT-PCR) to detect the effect of lncRNA on JEV proliferation. CCR1 was found to regulate the expression of lncRNA-NONSUST006715.1 by inhibitors screen. Transcription factor SP1 was overexpression or knockdown using RT-PCR to detect the influence of SP1 on the expression of lncRNA. In addition, the enrichments of transcription factor SP1 on the promoter of lncRNA-NONSUST006715.1 were analyzed by Chromatin immunoprecipitation.Results: In this study, we demonstrated a new function of lncRNA-NONSUST006715.1, the inhibition of JEV proliferation in PK-15 cells. We found that C-C chemokine receptor type 1 inhibited the expression of lncRNA-NONSUST006715.1 via the transcription factor SP1. Knockdown of CCR1 could upregulated the expression of SP1 and lncRNA-NONSUST006715.1, resulting in resistance to JEV proliferation. Conclusions: These findings illustrate the importance of lncRNAs in virus proliferation, and reveal how this virus regulates lncRNAs in host cells to promote its proliferation.

scholarly journals TIM-1 Promotes Japanese Encephalitis Virus Entry and Infection

Viruses ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 630 ◽  
Author(s):  
Jichen Niu ◽  
Ya Jiang ◽  
Hao Xu ◽  
Changjing Zhao ◽  
Guodong Zhou ◽  
...  
Keyword(s):  
Japanese Encephalitis Virus ◽  
Point Mutation ◽  
Japanese Encephalitis ◽  
Virus Entry ◽  
A549 Cells ◽  
Binding Pocket ◽  
Cytoplasmic Domain ◽  
Encephalitis Virus ◽  
Host Cells ◽  
Attachment Factor

Japanese encephalitis virus (JEV) is a mosquito-borne Flavivirus, the leading cause of viral-induced encephalitis. Several host molecules have been identified as the JEV attachment factor; however, the molecules involved in JEV entry remain poorly understood. In the present study, we demonstrate that TIM-1 is important for efficient infection by JEV. Firstly, three TIM-1 variants (V1, V2, and V3) were cloned from A549 cells, and we revealed that only ectopically TIM-1 V2 expression in 293T cells significantly promotes JEV attachment, entry and infection. Point mutation of phosphatidylserine (Ptdser) binding pocket in the TIM-1 IgV domain dampened JEV entry, indicating that TIM-1-mediated JEV infection is Ptdser-dependent. Furthermore, we found the cytoplasmic domain of TIM-1 is also required for enhancing JEV entry. Additionally, knock down of TIM-1 expression in A549 cells impaired JEV entry and infection, but not attachment, suggesting that additional factors exist in A549 cells that allow the virus to bind. In conclusion, our findings demonstrate that TIM-1 promotes JEV infection as an entry cofactor, and the polymorphism of TIM-1 is associated with JEV susceptibility to host cells.

scholarly journals Review of Emerging Japanese Encephalitis Virus: New Aspects and Concepts about Entry into the Brain and Inter-Cellular Spreading

Pathogens ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 111 ◽  
Author(s):  
Filgueira ◽  
Lannes
Keyword(s):  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Human Case ◽  
Encephalitis Virus ◽  
The Body ◽  
Host Cells ◽  
Asia Pacific ◽  
Latently Infected ◽  
The Impact ◽  
The Brain

Japanese encephalitis virus (JEV) is an emerging flavivirus of the Asia-Pacific region. More than two billion people live in endemic or epidemic areas and are at risk of infection. Recently, the first autochthonous human case was recorded in Africa, and infected birds have been found in Europe. JEV may spread even further to other continents. The first section of this review covers established and new information about the epidemiology of JEV. The subsequent sections focus on the impact of JEV on humans, including the natural course and immunity. Furthermore, new concepts are discussed about JEV’s entry into the brain. Finally, interactions of JEV and host cells are covered, as well as how JEV may spread in the body through latently infected immune cells and cell-to-cell transmission of virions or via other infectious material, including JEV genomic RNA.

scholarly journals The feasibility of field collected pig oronasal secretions as specimens for the virologic surveillance of Japanese encephalitis virus

2021 ◽  
Vol 15 (12) ◽  
pp. e0009977
Author(s):  
Shyan-Song Chiou ◽  
Jo-Mei Chen ◽  
Yi-Ying Chen ◽  
Min-Yuan Chia ◽  
Yi-Chin Fan
Keyword(s):  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Encephalitis Virus ◽  
Mosquito Vector ◽  
Rt Pcr ◽  
Viral Rnas ◽  
Epidemic Area ◽  
Route Of Transmission ◽  
Pig Farm ◽  
Blood Specimens

Virologic surveillance of Japanese encephalitis virus (JEV) relies on collecting pig blood specimens and adult mosquitoes in the past. Viral RNAs extracted from pig blood specimens suffer from low detecting positivity by reverse transcription PCR (RT-PCR). The oronasal transmission of the virus has been demonstrated in experimentally infected pigs. This observation suggested oronasal specimens could be useful source in the virus surveillance. However, the role of this unusual route of transmission remains unproven in the operational pig farm. In this study, we explore the feasibility of using pig oronasal secretions collected by chewing ropes to improve the positivity of detection in commercial pig farms. The multiplex genotype-specific RT-PCR was used in this study to determine and compare the positivity of detecting JEV viral RNAs in pig’s oronasal secretions and blood specimens, and the primary mosquito vector. Oronasal specimens had the overall positive rate of 6.0% (95% CI 1.3%–16.6%) (3/50) to 10.0% (95% CI 2.1%–26.5%) (3/30) for JEV during transmission period despite the negative results of all blood-derived specimens (n = 2442). Interestingly, pig oronasal secretions and female Culex tritaeniorhynchus mosquito samples collected from the same pig farm showed similar viral RNA positive rates, 10.0% (95% CI 2.1%–26.5%) (3/30) and 8.9% (95% CI 2.5%–21.2%) (4/45), respectively (p> 0.05). Pig oronasal secretion-based surveillance revealed the seasonality of viral activity and identified closely related genotype I virus derived from the mosquito isolates. This finding indicates oronasal secretion-based RT-PCR assay can be a non-invasive, alternative method of implementing JEV surveillance in the epidemic area prior to the circulation of virus-positive mosquitoes.

scholarly journals Rab5 and Rab11 Are Required for Clathrin-Dependent Endocytosis of Japanese Encephalitis Virus in BHK-21 Cells

2017 ◽  
Vol 91 (19) ◽  
Author(s):  
Chun-Chun Liu ◽  
Yun-Na Zhang ◽  
Zhao-Yao Li ◽  
Jin-Xiu Hou ◽  
Jing Zhou ◽  
...  
Keyword(s):  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Drug Targets ◽  
Encephalitis Virus ◽  
Dominant Negative ◽  
Endocytic Pathway ◽  
Host Cells ◽  
Rab Proteins ◽  
Endosomal Trafficking ◽  
Rab Gtpases

ABSTRACT During infection Japanese encephalitis virus (JEV) generally enters host cells via receptor-mediated clathrin-dependent endocytosis. The trafficking of JEV within endosomes is controlled by Rab GTPases, but which Rab proteins are involved in JEV entry into BHK-21 cells is unknown. In this study, entry and postinternalization of JEV were analyzed using biochemical inhibitors, RNA interference, and dominant negative (DN) mutants. Our data demonstrate that JEV entry into BHK-21 cells depends on clathrin, dynamin, and cholesterol but not on caveolae or macropinocytosis. The effect on JEV infection of dominant negative (DN) mutants of four Rab proteins that regulate endosomal trafficking was examined. Expression of DN Rab5 and DN Rab11, but not DN Rab7 and DN Rab9, significantly inhibited JEV replication. These results were further tested by silencing Rab5 or Rab11 expression before viral infection. Confocal microscopy showed that virus particles colocalized with Rab5 or Rab11 within 15 min after virus entry, suggesting that after internalization JEV moves to early and recycling endosomes before the release of the viral genome. Our findings demonstrate the roles of Rab5 and Rab11 on JEV infection of BHK-21 cells through the endocytic pathway, providing new insights into the life cycle of flaviviruses. IMPORTANCE Although Japanese encephalitis virus (JEV) utilizes different endocytic pathways depending on the cell type being infected, the detailed mechanism of its entry into BHK-21 cells is unknown. Understanding the process of JEV endocytosis and postinternalization will advance our knowledge of JEV infection and pathogenesis as well as provide potential novel drug targets for antiviral intervention. With this objective, we used systematic approaches to dissect this process. The results show that entry of JEV into BHK-21 cells requires a low-pH environment and that the process occurs through dynamin-, actin-, and cholesterol-dependent clathrin-mediated endocytosis that requires Rab5 and Rab11. Our work provides a detailed picture of the entry of JEV into BHK-21 cells and the cellular events that follow.

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