Frequency and clinical associations of Epstein-Barr virus molecular detection in systemic lupus erythematosus: A follow-up study

Abstract

Background

The “viral hypothesis” as an environmental factor that potentially triggers/modulates autoimmune diseases has been studied. Epstein-Barr virus (EBV) stands out as a relevant agent in the pathogenesis of systemic lupus erythematosus (SLE). Therefore, our aim was to evaluate the frequency of EBV molecular detection and its possible clinical and laboratory associations in a prospective cohort of SLE patients.

Methods

An observational prospective study was conducted and SLE patients were evaluated at two timepoints: baseline and after 6 months of follow-up. Clinical and laboratory data were collected from medical records and disease activity (SLEDAI-2K) and accumulated damage (SLICC-DI) scores were calculated. EBV-DNA was detected by real-time polymerase chain reaction (qPCR).

Results

We included 104 patients, 93.2% (n = 97) female with a mean age of 42.6 ± 13.45 years-old. At baseline, 39 (37.5%) patients presented detectable EBV-DNA and this frequency significantly increased at follow-up to 55.4% (p = .02). EBV detection was correlated with laboratory parameters, such as higher serum creatinine (p = .02), urea (p = .04) and ferritin (p = .04) at baseline. In patients with higher viral load (>1000 copies/mL), there was a slight increase in the median SLEDAI-2K (p = .07). Lastly, an age-adjusted logistic regression analysis indicated that immunosuppression at baseline was significantly associated with EBV-DNA positivity (OR = 2.86; 95%CI = 1.08-7.57; p = .03).

Conclusion

The significant increase in EBV positivity during the follow-up of SLE patients may indicate a dynamic variation of viral replication. Moreover, our findings suggest a possible association between EBV, renal manifestations and systemic inflammation in SLE. Finally, we identified that immunosuppression may favor viral replication.