Avian leukosis virus subgroup J and reticuloendotheliosis virus coinfection induced TRIM62 regulation of the actin cytoskeleton.
Actin Cytoskeleton
/ genetics
Animals
Avian Leukosis
/ physiopathology
Avian Leukosis Virus
/ physiology
Avian Proteins
/ genetics
Coinfection
/ physiopathology
Gene Expression Regulation
Poultry Diseases
/ physiopathology
Reticuloendotheliosis virus
/ physiology
Retroviridae Infections
/ physiopathology
Tripartite Motif Proteins
/ genetics
Avian leukosis virus subgroup J
TRIM62
actin cytoskeleton
coinfection
reticuloendotheliosis virus
Journal
Journal of veterinary science
ISSN: 1976-555X
Titre abrégé: J Vet Sci
Pays: Korea (South)
ID NLM: 100964185
Informations de publication
Date de publication:
May 2020
May 2020
Historique:
received:
10
01
2020
revised:
26
02
2020
accepted:
12
03
2020
entrez:
2
6
2020
pubmed:
2
6
2020
medline:
21
10
2020
Statut:
ppublish
Résumé
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. 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. 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. 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. 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.
Sections du résumé
BACKGROUND
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
OBJECTIVE
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
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
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
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.
Identifiants
pubmed: 32476322
pii: 21.e49
doi: 10.4142/jvs.2020.21.e49
pmc: PMC7263916
doi:
Substances chimiques
Avian Proteins
0
Tripartite Motif Proteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e49Subventions
Organisme : Natural Science Foundation of Shandong Province
ID : ZR2017MC011
Pays : China
Organisme : National Natural Science Foundation of China
ID : 31772703
Pays : China
Informations de copyright
© 2020 The Korean Society of Veterinary Science.
Déclaration de conflit d'intérêts
The authors declare no conflicts of interest.
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