Different viral exposures have been implicated in the etiology of rheumatoid arthritis (RA). Evidence relating to the association between putative viral exposures and the development of RA was reviewed.
A systematic literature search was conducted using MEDLINE-OVID, EMBASE-OVID, PUBMED and Cochrane library databases. Articles were included if they were case-controls, cross-sectional or cohort studies and were published in English. Case-series were included if there was a lack of other study designs.
Of 6724 citations, 48 were included in meta-analysis. Studies had poor quality. PBV19 infection was increased in RA compared to controls [N = 12, odds ratio (OR) 1.77 (95% CI: 1.11; 2.80) p = 0.02 for PVB19 IgG]. IgG anti-EBNA antibodies were not increased in RA (N = 17, p = 0.75), but anti-VCA [N = 18, OR 1.5 (95% CI: 1.07; 2.10), p = 0.02] and anti-EA antibodies [N = 11, OR 2.74 (95% CI: 1.27; 5.94), p = 0.01] were increased in RA. CMV was not associated with RA (N = 13, p = 0.42), nor was HBV (N = 5, p = 0.09). HCV was associated with RA in 7 case-control studies [OR 2.82 (95% CI: 1.35; 5.90), p = 0.006] and one cohort study [hazard ratio (HR) 2.03 (95% CI: 1.27, 3.22), p < 0.01]. Persistent arthritis was increased after Chikungunya fever [N = 2, OR 90 (95% CI: 15.2, 134.3), p = 0.047].
Studies of RA after viral exposures have poor quality. There is a risk of RA after Parvo B19, HCV and possibly EBV infection. CMV and HBV infections are not associated with RA. CHIKV is associated with the persistent inflammatory arthritis.