Long-Standing Rheumatoid Arthritis With Elevated Epstein–Barr Virus IgG Titers: A Case Report From India

TL;DR

A case report from India shows that a person with long-term rheumatoid arthritis has high Epstein-Barr virus antibodies, suggesting a possible link between the virus and the disease.

Contribution

This case provides region-specific evidence from India that EBV seropositivity persists in long-standing rheumatoid arthritis.

Findings

A 62-year-old woman with 20-year RA had persistently elevated EBV VCA IgG titers.

No RA flare or EBV reactivation was observed despite high antibody levels.

The case supports the idea that EBV may contribute to disease-specific humoral responses in RA.

Abstract

Rheumatoid arthritis (RA) is a systemic autoimmune disease with multifactorial etiology, and Epstein-Barr virus (EBV) has been proposed as an environmental trigger contributing to RA pathogenesis. Previous studies in India have shown that sera from early RA patients react to deiminated proteins encoded by EBV, with antibodies such as anti-viral citrullinated peptide (anti-VCP) and anti-EBNA-1 present exclusively in RA patients, suggesting a role for EBV in inducing disease-specific antibodies. Globally, RA patients demonstrate elevated antibodies against multiple EBV proteins, including VCA, EA, EBNA-1, and EBNA-2, independent of disease duration, activity, or treatment, and possess increased numbers of circulating EBV-infected B cells. Experimental and clinical evidence indicates that these antibodies, particularly anti-citrullinated collagen type II (CII) antibodies, may contribute to immune self-perpetuation and joint pathology. We report a 62-year-old woman with a 20-year history of seropositive RA, clinically stable on methotrexate and tofacitinib, who exhibited persistently elevated EBV viral capsid antigen (VCA) IgG titers (>750 U/mL), with asymptomatic trace proteinuria and microscopic haematuria. No RA flare or EBV reactivation was observed. This case provides region-specific evidence from India that complements prior studies, illustrating that EBV seropositivity persists in long-standing RA and may continue to contribute to disease-specific humoral responses. These findings underscore the need for longitudinal studies and advanced viral assays to clarify the role of EBV-related markers in RA pathogenesis.