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SAT0071 Dependence of rheumatoid arthritis disease aggressivity and activity on the presence of parvovirus B19 infection markers
  1. O. Bratslavska1,
  2. A. Kadisa2,
  3. S. Kozireva1,
  4. E. Pavlova1,
  5. N. Kakurina1,
  6. A. Lejnieks2,
  7. M. Murovska1
  1. 1A.Kirchenstein Institute of Microbiology & Virology
  2. 2Inner Diseases, Riga Stradins University, Riga, Latvia

Abstract

Background The role of parvovirus B19 (B19) infection as an initiator of the classic erosive rheumatoid arthritis (RA) is being constantly debated. The main argument against etiological association of B19 with RA is a very small portion of erosive arthritisregistered after acute B19 infection. However B19-associated RA may be developed as a consequence of persistent B19 infection in host’s tissues and a chronic immune activation.

Objectives To study a possible association between aggressivity and activity of RA clinical course and presence of B19 infection markers.

Methods Serum/plasma and blood samples from 52 RA patients (35 of them with erosive arthritis) and 25 sex and age-matched apparentlyhealthy individuals were studied. The values of rheumatoid factor (RF) and anti-cyclic citrullinated protein antibodies (anti-CCP) were analyzed as markers of RA aggressivity. The disease activity score (DAS), serum C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were analyzed as disease activity indicators. Virus-specific IgG and IgM class antibodies were detectedusing recomLine Parvovirus B19 IgG and IgM test, the presence of B19 genomic sequences - by B19 VP1 and B19 NS1 nested PCRs. Fisher’s exact test, the independent-samples T test and ANOVA were used in the statistical analyses.

Results The serological studies revealed anti-B19 IgG antibodies in 76% (19/25) of healthy individuals and 92.3% (48/52) of RA patients, the specific IgM antibodies werefound in 30.8% (16/52) of RA patients and 8% (2/25) of healthy persons (p=0.042), the presence of B19 DNA was detected in 26.9% (14/52) of RA patients and 12% (3/25) of control group individuals plasma DNA samples. 14 out of 52 RA patients had only virus specific IgG, 12 - IgM and IgG, 5 - IgM± and IgG class antibodies, in another 12 patients - virus-specific antibodies and viremia were revealed, in 5 - viral genomic sequences were detected in the blood cells’ DNA together with other B19 infection markers, but 4 patients were without B19 infection. The markers of active B19 infection (presence of anti-B19 IgM class antibodies and virus DNA in plasma or blood) were observed in 29/52 (55.8%) RA patients versus 4/25 (16.0%) control group individuals (p=0.0012). The indexes of disease activity (CRP and DAS but not ERS) were higher in patients with active B19 infection (IgM antibodies and virus DNA in plasma or blood cells) compare to the patients’ group with virus specific IgG class antibodies (IgG+) only. The mean values of the disease activity indexes in IgG+ group patients were DAS=3.94±0.31, CRP=3.97±0.58 mg/L versus DAS=5.42±0.26 (p<0.001), CRP=12.93±3.22 mg/L in thegroup with virus DNA in plasma or blood cells, and more high DAS=5.52±0.21 (p<0.001), CRP=47.31±9.73 mg/L (p<0.0001) in the IgM+ group patients. In the IgM+ group high indexes of disease aggressivity were observed: RF=267.37±59.64 U/ml and anti-CCP=398.60±120.11 U/ml versus RF=63.19±22.73 U/ml (p=0.006) and anti-CCP=71.22±45.59 U/ml (p=0.023) in the IgG+ group.

Conclusions The high frequency of B19 infection in RA patients and disease exacerbation upon active B19 infection are indicatives of the implication of B19 infection in RA ethiopathogenesis.

Disclosure of Interest None Declared

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