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TRIM62 From Chicken as a Negative Regulator of Reticuloendotheliosis Virus Replication.

ABSTRACT: Emerging evidence suggests that the tripartite motif containing 62 (TRIM62), a member of the TRIM family, plays an important role in antiviral processes. The objective of the study was to explore the role of TRIM62 in reticuloendotheliosis virus (REV) infection and its potential molecular mechanism. We first demonstrated that the REV infection affected the TRIM62 expression first upregulated and then downregulated in CEF cells. Next, we evaluated the effect of TRIM62 on viral replication. Overexpression of TRIM62 decreased REV replication. On the contrary, silencing of endogenously expressed TRIM62 increased viral replication. Then, to explore the necessity of domains in TRIM62's negative regulation on viral replication, we transfected CEF cells with TRIM62 domain deletion mutants. Deletion domain partially abolished TRIM62's antiviral activity. The effect of SPRY domain deletion was the highest and that of coiled-coil was the lowest. Further, we identified 18 proteins that coimmunoprecipitated and interacted with TRIM62 by immunocoprecipitation and mass spectrometry analysis. Strikingly, among which, both Ras-related protein Rab-5b (RAB5B) and Arp2/3 complex 34-kDa subunit (ARPC2) were involved in actin cytoskeletal pathway. Altogether, these results strongly suggest that chicken TRIM62 provides host defense against viral infection, and all domains are required for its action. RAB5B and ARPC2 may play important roles in its negative regulation processes.

SUBMITTER: Li L

PROVIDER: S-EPMC7146716 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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TRIM62 From Chicken as a Negative Regulator of Reticuloendotheliosis Virus Replication.

Li Ling L Niu Dongyan D Yang Jie J Bi Jianmin J Zhang Lingjuan L Cheng Ziqiang Z Wang Guihua G

Frontiers in veterinary science 20200403

Emerging evidence suggests that the tripartite motif containing 62 (TRIM62), a member of the TRIM family, plays an important role in antiviral processes. The objective of the study was to explore the role of TRIM62 in reticuloendotheliosis virus (REV) infection and its potential molecular mechanism. We first demonstrated that the REV infection affected the TRIM62 expression first upregulated and then downregulated in CEF cells. Next, we evaluated the effect of TRIM62 on viral replication. Overex ...[more]

PMID: 32318585

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Project description:BACKGROUND:Coinfection with avian leukosis virus subgroup J (ALV-J) and reticuloendotheliosis virus (REV) is common in chickens, and the molecular mechanism of the synergistic pathogenic effects of the coinfection is not clear. Exosomes have been identified as new players in the pathogenesis of retroviruses. The different functions of exosomes depend on their cargo components. OBJECTIVES:The aim of this study was to investigate the function of co-regulation differentially expressed proteins in exosomes on coinfection of ALV-J and REV. METHODS:Here, viral replication in CEF cells infected with ALV-J, REV or both was detected by immunofluorescence microscopy. Then, we analyzed the exosomes isolated from supernatants of chicken embryo fibroblast (CEF) cells single infected and coinfected with ALV-J and REV by mass spectrometry. KEGG pathway enrichment analyzed the co-regulation differentially expressed proteins in exosomes. Next, we silenced and overexpressed tripartite motif containing 62 (TRIM62) to evaluate the effects of TRIM62 on viral replication and the expression levels of NCK-association proteins 1 (NCKAP1) and actin-related 2/3 complex subunit 5 (ARPC5) determined by quantitative reverse transcription polymerase chain reaction. RESULTS:The results showed that coinfection of ALV-J and REV promoted the replication of each other. Thirty proteins, including TRIM62, NCK-association proteins 1 (NCKAP1, also known as Nap125), and Arp2/3-5, ARPC5, were identified. NCKAP1 and ARPC5 were involved in the actin cytoskeleton pathway. TRIM62 negatively regulated viral replication and that the inhibition of REV was more significant than that on ALV-J in CEF cells coinfected with TRIM62. In addition, TRIM62 decreased the expression of NCKAP1 and increased the expression of ARPC5 in coinfected CEF cells. CONCLUSIONS:Collectively, our results indicated that coinfection with ALV-J and REV competitively promoted each other's replication, the actin cytoskeleton played an important role in the coinfection mechanism, and TRIM62 regulated the actin cytoskeleton.

Dataset Information

TRIM62 From Chicken as a Negative Regulator of Reticuloendotheliosis Virus Replication.

Publications

TRIM62 From Chicken as a Negative Regulator of Reticuloendotheliosis Virus Replication.

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