Retrovirus implicated in Rheumatoid Arthritis

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Retrovirus implicated in Rheumatoid Arthritis

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Human Endogenous Retrovirus Implicated in Rheumatoid Arthritis




NEW YORK (Reuters Health) May 01 - Expression of human endogenous retrovirus (HERV)-K10 mRNA is higher in patients with rheumatoid arthritis (RA) compared with healthy control subjects or patients with osteoarthritis, British scientists report, suggesting that the virus is somehow associated with the pathogenesis of this autoimmune disease.

According to their paper in the May issue of the Annals of the Rheumatic Diseases, approximately 8% of the human genome is derived from HERV, which is transmitted vertically through the germline. Rarely, HERV-K viral particles may be produced.

However, the research team, led by Dr. Hora Davari Ejtehadi from the University of Wolverhampton, found only a few published reports in which direct molecular approaches were used to detect and quantify the presence of HERV mRNA in patients with RA compared with control subjects.

They therefore developed a novel multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) system to measure the level of HERV-K10 mRNA expression in peripheral blood mononuclear cells (PBMCs). Southern blot and DNA sequencing, compared with the published HERV-K10 reference sequence, were used to confirm the authenticity of the PCR products.

To explore the relationship between HERV and RA, the researchers analyzed PBMCs from 40 patients with RA, 17 with osteoarthritis, and 27 controls. Levels of HERV-K10 were compared with those of the housekeeping gene histidyl tRNA synthetase.

Results showed that of 68% of PBMCs from RA patients had increased HERV-K10 mRNA expression levels compared with the housekeeping gene, versus 17% of PBMCs from patients with osteoarthritis and 18.5% of PBMCs from controls (p = 0.02 for both).

According to Dr. Ejtehadi's group, the effects of increased HERV in RA may be related to HERV's molecular mimicry of host proteins, superantigen motifs that bypass T cell restriction, or environmental triggers that activate HERVs. Host cells with activated HERV may then migrate to the synovium, where they release pro-inflammatory cytokines.

Ann Rheum Dis 2006;65:612-616.




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