Parvovirus B19 NS1 protein induces synovitis mimicking rheumatoid arthritis

This study aims to investigate the role of parvovirus B19 infection in the pathogenesis of rheumatoid arthritis (RA). B19-NS1 DNA was cloned into the LentiORF pLEX-MCS vector, then co-transfected with the pLEX-MCS-NS1 vector and packaging system to produce LEX-NS1 lentiviral stock. LEX was also prep...

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Published inScientific reports Vol. 15; no. 1; pp. 28679 - 11
Main Authors Yen, Chang-Yi, Tseng, Chia-Chun, Lin, Chia‐Hui, Lin, Yuan‐Zhao, Li, Ruei‐Nian, Wang, Pin-Yi, Chen, Kuan-Yu, Wu, Cheng-Chin, Ou, Tsan-Teng, Chen, Chung-Jen, Liu, Yu-Peng, Yen, Jeng-Hsien
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Abstract This study aims to investigate the role of parvovirus B19 infection in the pathogenesis of rheumatoid arthritis (RA). B19-NS1 DNA was cloned into the LentiORF pLEX-MCS vector, then co-transfected with the pLEX-MCS-NS1 vector and packaging system to produce LEX-NS1 lentiviral stock. LEX was also prepared as the control. Transduction of LEX-NS1 or LEX lentivirus into the SW982 cell line then proceeded, and total RNA was extracted for RNA-seq. Pathway analysis and comparison of pathway status between this study and GEO datasets were performed, demonstrating that acute phase response signaling, NRF2-mediated oxidative stress response, and mTOR signaling pathways were activated after the transduction of LEX-NS1 into the SW982 cell line, although the interferon signaling pathway was inhibited. The comparison of all pathways using hierarchical clustering showed that the pathway status after transduction of B19-NS1 was closer to RA than that in osteoarthritis. Similar findings can also be found in cellular immune, humoral immune, cytokine, apoptosis, cellular growth, cellular stress, growth factor, and intracellular pathways. In conclusion, parvovirus B19-NS1 can induce inflammation of the synovium mimicking synovitis in RA; therefore, parvovirus B19 infection might be one of the trigger factors in the pathogenesis of RA.
AbstractList Abstract This study aims to investigate the role of parvovirus B19 infection in the pathogenesis of rheumatoid arthritis (RA). B19-NS1 DNA was cloned into the LentiORF pLEX-MCS vector, then co-transfected with the pLEX-MCS-NS1 vector and packaging system to produce LEX-NS1 lentiviral stock. LEX was also prepared as the control. Transduction of LEX-NS1 or LEX lentivirus into the SW982 cell line then proceeded, and total RNA was extracted for RNA-seq. Pathway analysis and comparison of pathway status between this study and GEO datasets were performed, demonstrating that acute phase response signaling, NRF2-mediated oxidative stress response, and mTOR signaling pathways were activated after the transduction of LEX-NS1 into the SW982 cell line, although the interferon signaling pathway was inhibited. The comparison of all pathways using hierarchical clustering showed that the pathway status after transduction of B19-NS1 was closer to RA than that in osteoarthritis. Similar findings can also be found in cellular immune, humoral immune, cytokine, apoptosis, cellular growth, cellular stress, growth factor, and intracellular pathways. In conclusion, parvovirus B19-NS1 can induce inflammation of the synovium mimicking synovitis in RA; therefore, parvovirus B19 infection might be one of the trigger factors in the pathogenesis of RA.
This study aims to investigate the role of parvovirus B19 infection in the pathogenesis of rheumatoid arthritis (RA). B19-NS1 DNA was cloned into the LentiORF pLEX-MCS vector, then co-transfected with the pLEX-MCS-NS1 vector and packaging system to produce LEX-NS1 lentiviral stock. LEX was also prepared as the control. Transduction of LEX-NS1 or LEX lentivirus into the SW982 cell line then proceeded, and total RNA was extracted for RNA-seq. Pathway analysis and comparison of pathway status between this study and GEO datasets were performed, demonstrating that acute phase response signaling, NRF2-mediated oxidative stress response, and mTOR signaling pathways were activated after the transduction of LEX-NS1 into the SW982 cell line, although the interferon signaling pathway was inhibited. The comparison of all pathways using hierarchical clustering showed that the pathway status after transduction of B19-NS1 was closer to RA than that in osteoarthritis. Similar findings can also be found in cellular immune, humoral immune, cytokine, apoptosis, cellular growth, cellular stress, growth factor, and intracellular pathways. In conclusion, parvovirus B19-NS1 can induce inflammation of the synovium mimicking synovitis in RA; therefore, parvovirus B19 infection might be one of the trigger factors in the pathogenesis of RA.
This study aims to investigate the role of parvovirus B19 infection in the pathogenesis of rheumatoid arthritis (RA). B19-NS1 DNA was cloned into the LentiORF pLEX-MCS vector, then co-transfected with the pLEX-MCS-NS1 vector and packaging system to produce LEX-NS1 lentiviral stock. LEX was also prepared as the control. Transduction of LEX-NS1 or LEX lentivirus into the SW982 cell line then proceeded, and total RNA was extracted for RNA-seq. Pathway analysis and comparison of pathway status between this study and GEO datasets were performed, demonstrating that acute phase response signaling, NRF2-mediated oxidative stress response, and mTOR signaling pathways were activated after the transduction of LEX-NS1 into the SW982 cell line, although the interferon signaling pathway was inhibited. The comparison of all pathways using hierarchical clustering showed that the pathway status after transduction of B19-NS1 was closer to RA than that in osteoarthritis. Similar findings can also be found in cellular immune, humoral immune, cytokine, apoptosis, cellular growth, cellular stress, growth factor, and intracellular pathways. In conclusion, parvovirus B19-NS1 can induce inflammation of the synovium mimicking synovitis in RA; therefore, parvovirus B19 infection might be one of the trigger factors in the pathogenesis of RA.This study aims to investigate the role of parvovirus B19 infection in the pathogenesis of rheumatoid arthritis (RA). B19-NS1 DNA was cloned into the LentiORF pLEX-MCS vector, then co-transfected with the pLEX-MCS-NS1 vector and packaging system to produce LEX-NS1 lentiviral stock. LEX was also prepared as the control. Transduction of LEX-NS1 or LEX lentivirus into the SW982 cell line then proceeded, and total RNA was extracted for RNA-seq. Pathway analysis and comparison of pathway status between this study and GEO datasets were performed, demonstrating that acute phase response signaling, NRF2-mediated oxidative stress response, and mTOR signaling pathways were activated after the transduction of LEX-NS1 into the SW982 cell line, although the interferon signaling pathway was inhibited. The comparison of all pathways using hierarchical clustering showed that the pathway status after transduction of B19-NS1 was closer to RA than that in osteoarthritis. Similar findings can also be found in cellular immune, humoral immune, cytokine, apoptosis, cellular growth, cellular stress, growth factor, and intracellular pathways. In conclusion, parvovirus B19-NS1 can induce inflammation of the synovium mimicking synovitis in RA; therefore, parvovirus B19 infection might be one of the trigger factors in the pathogenesis of RA.
This study aims to investigate the role of parvovirus B19 infection in the pathogenesis of rheumatoid arthritis (RA). B19-NS1 DNA was cloned into the LentiORF pLEX-MCS vector, then co-transfected with the pLEX-MCS-NS1 vector and packaging system to produce LEX-NS1 lentiviral stock. LEX was also prepared as the control. Transduction of LEX-NS1 or LEX lentivirus into the SW982 cell line then proceeded, and total RNA was extracted for RNA-seq. Pathway analysis and comparison of pathway status between this study and GEO datasets were performed, demonstrating that acute phase response signaling, NRF2-mediated oxidative stress response, and mTOR signaling pathways were activated after the transduction of LEX-NS1 into the SW982 cell line, although the interferon signaling pathway was inhibited. The comparison of all pathways using hierarchical clustering showed that the pathway status after transduction of B19-NS1 was closer to RA than that in osteoarthritis. Similar findings can also be found in cellular immune, humoral immune, cytokine, apoptosis, cellular growth, cellular stress, growth factor, and intracellular pathways. In conclusion, parvovirus B19-NS1 can induce inflammation of the synovium mimicking synovitis in RA; therefore, parvovirus B19 infection might be one of the trigger factors in the pathogenesis of RA.
ArticleNumber 28679
Author Chen, Chung-Jen
Liu, Yu-Peng
Lin, Yuan‐Zhao
Wu, Cheng-Chin
Tseng, Chia-Chun
Wang, Pin-Yi
Ou, Tsan-Teng
Chen, Kuan-Yu
Yen, Jeng-Hsien
Lin, Chia‐Hui
Li, Ruei‐Nian
Yen, Chang-Yi
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Issue 1
Keywords Synovitis
RNA-seq
Rheumatoid arthritis
Parvovirus B19
Language English
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Snippet This study aims to investigate the role of parvovirus B19 infection in the pathogenesis of rheumatoid arthritis (RA). B19-NS1 DNA was cloned into the LentiORF...
Abstract This study aims to investigate the role of parvovirus B19 infection in the pathogenesis of rheumatoid arthritis (RA). B19-NS1 DNA was cloned into the...
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SubjectTerms 692/4023
692/699/1670/498
Apoptosis
Arthritis, Rheumatoid - etiology
Arthritis, Rheumatoid - metabolism
Arthritis, Rheumatoid - pathology
Arthritis, Rheumatoid - virology
Autoimmune diseases
Cell Line
Cellular stress response
Cytokines
Datasets
Enzymes
Growth factors
Humanities and Social Sciences
Humans
Infections
Inflammation
Kinases
Mimicry
multidisciplinary
NS1 protein
Osteoarthritis
Oxidative stress
Parvoviridae Infections - complications
Parvoviridae Infections - virology
Parvovirus B19
Parvovirus B19, Human - genetics
Parvovirus B19, Human - metabolism
Parvoviruses
Pathogenesis
Proteins
Rheumatoid arthritis
RNA-seq
Science
Science (multidisciplinary)
Signal Transduction
Standard scores
Synovitis
Synovitis - etiology
Synovitis - metabolism
Synovitis - pathology
Synovitis - virology
Synovium
TOR protein
Viral infections
Viral Nonstructural Proteins - genetics
Viral Nonstructural Proteins - metabolism
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Title Parvovirus B19 NS1 protein induces synovitis mimicking rheumatoid arthritis
URI https://link.springer.com/article/10.1038/s41598-025-11900-3
https://www.ncbi.nlm.nih.gov/pubmed/40770277
https://www.proquest.com/docview/3237114654
https://www.proquest.com/docview/3237451194
https://pubmed.ncbi.nlm.nih.gov/PMC12328570
https://doaj.org/article/2079ee8908bc421fb1866c0dbfd2c2ba
Volume 15
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