Background The pathogenesis of rheumatoid arthritis (RA) involves genetic, immunological and environmental factors. The main risk factors for RA are the presence of the shared epitope (SE) alleles, anti-cyclic citrullinated peptide (Anti-CCP) antibodies and smoking. The role of the virus is controversial and not fully understood. There is some evidence that Epstein-Barr virus (EBV) load is increased in patients with RA, but it is still not elucidated if EBV is directly involved in the immunopathogenesis of RA or high EBV load in patients is due their defective immune control.
Some basic research suggests that EBV could interact with SE alleles, anti-CCP antibodies or smoking, increasing the risk for RA. However there is no clinical studies proving an association between EBV and the main risk factors for RA.
Objectives The objective of this study is to establish whether there are associations among EBV load, SE alleles, anti-CCP antibodies and smoking in Brazilian patients with RA. Secondary objectives include a comparative analysis of EBV load and the main risk factors for RA in patients and healthy controls.
Methods In this case-control study, we included 140 Brazilian patients with RA and 143 healthy controls; matched for age, sex and ethnicity. We performed a clinical and laboratory characterization of the sample. Genotyping was performed to identify SE alleles, anti-CCP antibodies were examined by ELISA and smoking information was collected from all subjects. To quantify the viral load of EBV, we performed the quantitative method of polymerase chain reaction in real time (real-time PCR).
Results The quantification of EBV load by real-time PCR proved to be significantly higher in patients than in controls (graph, p<0.001). Comparative analysis among the groups also showed a significantly higher positivity for the alleles of SE, anti-CCP antibodies and smoking in patients (table).
Association analysis showed that positivity of anti-CCP antibodies was higher in patients with SE alleles which are smoker or ex-smoker (p=0.038). However, there were no associations among EBV viral load and SE, anti-CCP antibodies or smoking status of patients.
Conclusions Although patients with RA have an increased EBV viral load, this study did not associate EBV load with the main risk factors for RA. We suggest that these findings may be due to a deficient control of EBV in patients with RA. Therefore, it is not possible to establish a direct causal relationship between EBV and RA, remaining controversial the role of this virus in RA pathogenesis.
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Disclosure of Interest None declared
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