High prevalence of immunoglobulin A antibody against Epstein-Barr virus capsid antigen in adult patients with lupus with disease flare: case control studies.
OBJECTIVE
Systemic lupus erythematosus (SLE) is a severe autoimmune disease with rare remission and recurrent flare. Epstein-Barr virus (EBV) infection has been reported to be strongly associated with SLE in the United States, but with an inconclusive role in Asia. We investigated the role of EBV infection in patients with SLE in Taiwan, with one of the highest population densities in Asia.


METHODS
We conducted case-control studies to test whether EBV infection was associated with adult SLE in Taiwan. In the first study, 36 adults with SLE and 36 sex and age matched controls were enrolled for examination of serum IgG, IgM, and IgA antibody against EBV-virus capsid antigen (EBV-VCA). In the second study, another 36 adult lupus cases and 36 matched controls were enrolled to confirm the high prevalence of IgA antibody against EBV-VCA found in the first study. Further, both groups of SLE patients were combined to analyze the association between the existence of IgA antibody against EBV-VCA and disease activity (determined by SLEDAI score) and disease flare in patients with SLE.


RESULTS
In the first study, IgA antibody against EBV-VCA was the only marker with significantly higher prevalence in adults with SLE compared to healthy adults (36.1% vs 5.6%; p < 0.005). In the second study, we confirmed that the prevalence of IgA antibody against EBV-VCA was indeed higher in adults with SLE (38.9% vs 2.8%; p < 0.001). With further analysis (pooling analysis), adult SLE patients with IgA antibody against EBV-VCA had higher disease activity compared to SLE patients without IgA antibody against EBV-VCA (SLEDAI 7.8 +/- 6.6 vs 3.3 +/- 2.1; p < 0.001). SLE patients with flare showed much higher prevalence of IgA antibody against EBV-VCA compared to those without flare (81.3% vs 25.0%; p < 0.001).


CONCLUSIONS
This is the first evidence that IgA antibody against EBV-VCA is strongly associated with disease flare in SLE patients. It suggests that EBV reactivation may contribute toward the disease flare of SLE.
Chen
Chung-Jen
CJ
Department of Internal Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Lin
Kuei-Hsiang
KH
Lin
Shih-Chang
SC
Tsai
Wen-Chan
WC
Yen
Jeng-Hsien
JH
Chang
Shun-Jen
SJ
Lu
Sheng-Nan
SN
Liu
Hong-Wen
HW
D000328:Adult; D000914:Antibodies, Viral / Q000276:immunology; D000956:Antigens, Viral / Q000276:immunology; D002213:Capsid / Q000276:immunology; D036022:Capsid Proteins / Q000276:immunology; D016022:Case-Control Studies; D020031:Epstein-Barr Virus Infections / Q000150:complications* / Q000453:epidemiology / Q000276:immunology; D005260:Female; D004854:Herpesvirus 4, Human / Q000276:immunology / Q000302:isolation & purification*; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000453:epidemiology / Q000276:immunology / Q000821:virology*; D008297:Male; D012008:Recurrence; D016036:Seroepidemiologic Studies; D013624:Taiwan / Q000453:epidemiology
D000914:Antibodies, Viral; D000956:Antigens, Viral; D036022:Capsid Proteins; C041788:Epstein-Barr viral capsid antigen; D007070:Immunoglobulin A; D007075:Immunoglobulin M