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AB0079 Demonstration of Parvovirus B19 Infection in Rheumatoid Arthritis
  1. A. Kadisa1,
  2. S. Kozireva2,
  3. O. Bratslavska1,
  4. V. Groma3,
  5. P. Studers4,
  6. A. Lejnieks5,
  7. M. Murovska2
  1. 1A.Kirchenstein Institute of Microbiology and Virology
  2. 2A.Kirchenstein Institute of Microbiology and Virology, Riga Stradins University
  3. 3Institute of Anatomy and Anthropology, Riga Stradins University
  4. 4Traumatology and Orthopaedics Hospital
  5. 5Department of Internal Diseases, Riga Stradins University, Riga, Latvia


Background The exact cause of the rheumatoid arthritis (RA) is not known. Parvovirus B19 (B19) is one of the most perspective candidates in capacity of etiological agent of RA. Evidence implicating B19 in RA causation is conflicting, but several reports have clearly confirmed its role in the pathogenesis of RA.

Objectives In this study we detect the presence of B19 infection markers and the spectra of synovial and supporting tissue damage in RA patients.

Methods 52 RA patients and 25 age and gender matched healthy individuals were enrolled in this study and peripheral blood samples collected. RecomLine test was used to detect of B19-specific antibodies, nPCR – to detect virus-specific sequences and proliferation test – to detect PBMC response to B19 antigens. Patients' synovial, cartilaginous and osseous samples from 7 RA patients were obtained and conventionally processed for histopathology. B19 capsid proteins VP1/VP2 expression was assessed by immunohistochemistry.

Results The markers of active B19 infection were found in 26.9% (14/52) RA patients in comparison with 8.0% (2/25) control group's individuals. Anti-B19 IgG class antibodies were detected in 76% of healthy persons and in 92.3% of RA patients. In control subjects the antibodies to no more than four B19 antigens were found. 38.5% (20/52) RA patients had also antibodies to B19 non-structural protein NS1 (p=0.001 in comparison with control group's individuals). The presence of viral genomic sequence in DNA from cell-free blood plasma was detected in 25% (13/52) of RA patients and 4% (1/25) of healthy individuals. On the 3rd day of cultivation in the presence of B19 antigens PBMC proliferation was observed in 48.0% (25/52) of RA patients and only in 8.0% (2/25) of healthy persons (p=0.00068). On the 6th day of cultivation PBMC of 63.5% (33/52) of RA patients and 32.0% (8/25) of control individuals responded to B19 antigens (p=0.01436). The PBMC of both control group persons with active B19 infection and 74.1% (10/14) of RA patients with the active virus infection had reacted to B19 antigens by proliferation on the 3rd day. Proliferative response to B19 antigens on the 3rd day was detected also in 44.8% (13/29) remotely infected RA patients while in control group no response was found in remotely infected persons (p=0.00071), but on the 6th day PBMC proliferative response to B19 antigens among remotely infected persons was detected in 68.9% (20/29) RA patients and 41.1% (6/17) control group's patients, respectively (p=0.0347). B19 capsid proteins' VP1/VP2 expression was confirmed as nuclear staining demonstrated in the sublining infiltrating cells and fibroblast-like synoviocytes in the intimal lining.

Conclusions The high frequency of active B19 infection markers, increased PBMC proliferative response to B19 antigens and B19 antigen expression detected in RA patients' synovial, cartilaginous and osseous tissues suggest that B19 infection is involved in the RA development and course. Affection of fibroblast-like synoviocytes may promote further behaviour changes contribute to disease mechanisms.

Disclosure of Interest None declared

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