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.

Scientific Reports
|August 6, 2025
PubMed

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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