Epstein-Barr virus and rheumatoid arthritis

[pattismith]

Epstein-Barr virus and rheumatoid arthritis
Author links open overlay panel NathalieBalandraudabJeanRoudierab
August 2017, Pages

Abstract
Rheumatoid arthritis (RA) is one of the most common autoimmune diseases, with a 0.5% worldwide prevalence.
The cause of RA remains unknown, however both genetic and environmental factors may contribute to its development.
Among these is the Epstein-Barr virus (EBV).
Here, we discuss several aspects of the close relationship between EBV and RA.
Patients with RA have impaired control of EBV infection. Indeed, they have high titres of antibodies against EBV antigens. Their peripheral blood T lymphocytes are less efficient at controlling the outgrowth of EBV-infected B cells. RA patients have more EBV-infected B cells than normal controls, leading to a 10-fold systemic EBV overload.

Post-transplant lymphoproliferative disorder (PTLPD) is a polyclonal EBV-positive B lymphocyte proliferation, which can evolve into an EBV-positive B cell lymphoma.

RA patients also have an increased risk of developing EBV-associated lymphoproliferative disorder (LPD). Hence the need to monitor EBV load when treating RA patients with immunosuppressors. EBV, a widespread virus, highly recognized by antibodies but never eliminated, is an ideal candidate to trigger chronic immune complex disease.

Anti-EBV antibody responses should be considered as one of the chronic autoantibody responses linked to the development of RA, in the same way as anti-citrullinated protein antibodies.

 

[Gemini]

The cause of RA remains unknown, however both genetic and environmental factors may contribute to its development. Among these is the Epstein-Barr virus (EBV). Here, we discuss several aspects of the close relationship between EBV and RA.

Patients with RA have impaired control of EBV infection. Indeed, they have high titres of antibodies against EBV antigens. Their peripheral blood T lymphocytes are less efficient at controlling the outgrowth of EBV-infected B cells. RA patients have more EBV-infected B cells than normal controls, leading to a 10-fold systemic EBV overload.

Thanks for posting this interesting abstract @pattismith.

Have been curious about B cells ability to harbor EBV, HHV-6, enteroviruses, etc. for some time.

Always appreciate @Jonathan Edwards thoughts and expertise. Wonder if he would comment on this paper and how this might play a role in ME/CFS and rituximab?

 

[pattismith]

ORIGINAL RESEARCH ARTICLE

Front. Immunol., 30 October 2020 | https://doi.org/10.3389/fimmu.2020.590444

Serological Evidence for the Association Between Epstein-Barr Virus Infection and Sjögren’s Syndrome

Jingxiu Xuan1,2†,

Zhiqian Ji1†, Bin Wang1†,

Xiaoli Zeng1,

Rongjuan Chen1,2, Yan He1,2,

Peishi Rao1,2, Puqi Wu1,2 and Guixiu Shi1,2*

• 1Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, China
• 2Department of Science & Technology, Xiamen Key Laboratory of Rheumatology and Clinical Immunology, Xiamen, China

Background:

Exposure to Epstein-Barr virus (EBV) infection has been hypothesized to be an important risk factor for multiple rheumatic diseases, but the serological evidence so far for its role in Sjögren’s syndrome (SjS) is not clearly established yet. This study aimed to assess the seroepidemiological associations of antibodies to EBV with SjS.

Methods:

A seroepidemiological study containing 119 patients with SjS and 65 healthy controls was first performed, in which the associations of SjS with four commonly studied EBV antibodies including IgM-anti-viral capsid antigen (anti-VCA) antibody, IgG-anti-VCA antibody, IgG-anti-early antigen (anti-EA) antibody, and IgG-anti-EBV nuclear antigen 1 (anti-EBNA1) antibody were evaluated. A systematic review and meta-analysis of eligible seroepidemiological studies was also carried out, and data syntheses were performed using random-effect meta-analysis.

Results:

In the case-control study, the patients with SjS had both a significantly higher prevalence of IgG-anti-EA antibody positivity (31.9% vs. 3.1%, P < 0.001) and high titers of IgG-anti-EA antibody (P < 0.001) than healthy controls.

The titer of IgG-anti-VCA antibody was significantly increased in the patients with SjS compared with healthy controls (P < 0.001).

IgG-anti-EA antibody seropositive patients with SjS had lower levels of both C3 (P = 0.002) and C4 (P = 0.02), and the titer of IgG-anti-EA antibody was inversely related to the levels of both C3 (r = -0.31, P < 0.001) and C4 (r = -0.20, P = 0.03).

A total of 14 eligible studies on the serological associations between EBV infection and SjS were finally included into the meta-analysis, which suggested obvious associations of SjS with IgM-anti-VCA antibody [Odds ratio (OR) = 5.77, 95%CI 1.73–19.25, P = 0.004] and IgG-anti-EA antibody (OR = 9.97, 95%CI 4.58-21.67, P < 0.00001).

Conclusions:

The findings from this study provide strong serological evidence for the association between EBV infection and SjS.

SjS has obvious associations with IgM-anti-VCA antibody and IgG-anti-EA antibody.

IgG-anti-EA antibody is linked to low levels of C3 and C4 in the patients with SjS, the significance of which needs to be addressed in further studies.