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Updated: Sep 12, 2025

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Parvovirus B19 NS1 protein induces synovitis mimicking rheumatoid arthritis
Chang-Yi Yen1,2, Chia-Chun Tseng1,3, Chia-Hui Lin1
1Division of Rheumatology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, 807, Taiwan.
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.
Insights
Parvovirus B19 infection, specifically the B19-NS1 protein, may trigger rheumatoid arthritis (RA) by inducing synovitis. This study found B19-NS1 activates pathways similar to RA pathogenesis.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation.
- The etiology of RA remains incompletely understood, with potential roles for infectious agents being investigated.
Purpose of the Study:
- To investigate the potential role of parvovirus B19 infection in the pathogenesis of rheumatoid arthritis (RA).
- To determine if the parvovirus B19 non-structural protein 1 (B19-NS1) can induce cellular changes mimicking RA synovitis.
Main Methods:
- Cloning of B19-NS1 DNA into a lentiviral vector (LentiORF pLEX-MCS).
- Transduction of the SW982 cell line with B19-NS1 lentivirus or control lentivirus.
- RNA sequencing (RNA-seq) and subsequent pathway analysis.
- Comparison of pathway status with existing rheumatoid arthritis and osteoarthritis datasets.
Main Results:
- Transduction with B19-NS1 activated key signaling pathways including acute phase response, NRF2-mediated oxidative stress, and mTOR signaling.
- The interferon signaling pathway was inhibited by B19-NS1 transduction.
- Pathway analysis indicated that B19-NS1 induced changes more closely resembling RA than osteoarthritis.
- B19-NS1 influenced pathways related to immune response, apoptosis, cellular growth, and stress.
Conclusions:
- Parvovirus B19 non-structural protein 1 (B19-NS1) can induce synovial inflammation, mimicking the synovitis observed in rheumatoid arthritis.
- Parvovirus B19 infection is proposed as a potential trigger factor in the pathogenesis of rheumatoid arthritis.
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