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SAT0339 Virologic and Morphologic Evidences of Human Parvovirus B19 Infection in Osteoarthritis
  1. A. Kadisa1,2,
  2. V. Groma3,
  3. S. Skuja3,
  4. M. Tarasovs3,
  5. O. Bratslavska1,
  6. S. Kozireva1,
  7. P. Studers4,
  8. A. Lejnieks2,
  9. M. Murovska1
  2. 2Department of Internal Diseases, Riga Stradins University
  3. 3Institute of Anatomy and Anthropology, Riga Stradins University
  4. 4Traumatology and Orthopaedics Hospital, Riga, Latvia


Background Viral infections play a role in the pathogenesis of various forms of osteoarthritis (OA). The advanced stage of disease often manifests with severe inflammation and lesions of joint tissues related to the parvovirus B19 (B19) infection.

Objectives This study aimed to demonstrate the spectra of synovial and supporting tissue damage in OA patients in association with the presence of B19 infection markers.

Methods 60 OA patients and 27 age and gender matched practically healthy persons were enrolled in this study and peripheral blood (PB) samples collected. RecomLine test was used to detect of B19-specific antibodies, nPCR – to detect virus-specific sequences, proliferation test – to detect T-lymphocytes’ response to B19 antigens. From 30OA patients synovial, cartilaginous and osseous samples were obtained and conventionally processed for histopathology. B19 capsid proteins’ VP1/VP2 expression and joint tissue remodeling was assessed by immunohistochemistry, COX2 mRNA expression – by RT-PCR.

Results Application of serological, molecular and immunohistochemical techniques sets up the presence of greatly varying results. No difference in the B19 specific IgG antibodies’ prevalence was found between OA patients and control group persons (83.3 and 76%, respectively), however antibodies to B19 NS1 were detected in 41.7% of OA patients vs. 3.7% of healthy persons. Anti-B19 IgM antibodies were revealed in OA patients significantly more often (30.5 vs. 8% in healthy persons). In peripheral blood/plasma DNA of 11 OA patients (18.3%) B19 genomic sequences were found. B19 sequences in PB leukocytes’ DNA were detected in OA patients only (7.7%). T-lymphocytes of OA patients responded to B19 antigens with proliferation more often and faster than control group persons confirming chronic activation of the first ones. Findings of B19 specific sequences in OA patients’ synovial tissues DNA were not unequivocal. B19 capsid protein expression was demonstrated in OA patients’ synovial, cartilaginous and osseous tissues. The red bone marrow erythroblasts, monocytes, megakaryocytes and endothelial cells showed affection evidenced by anti-B19 immunostaining. Inflammatory cells of synovial infiltrates also displayed the immunopositivity. The damage and remodeling of joint tissue was evidenced by strong immunoexpression of metalloproteinase-9 and transforming growth factor-beta found in the spongy bone, articular cartilage and synovial membrane compartments. In synovial tissues of OA patients with plasma viremia two times higher COX2 mRNA expression was shown in comparison with OA patients without viremia.

Conclusions We suggest that B19 infection may contribute to the inflammatory and structural damage in the advanced stage of OA. The results proved by application of serological and molecular biological B19 infection markers should not be considered solely. These findings should be jointly implemented by immunohistochemistry data reflecting the local tissue damage and contribution of B19 to OA.

Disclosure of Interest None Declared

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