In the Journals

Epstein-Barr virus infection contributed to SLE development

Epstein-Barr virus infection contributed to the development of systemic lupus erythematosus, according to a recent systematic review and meta-analyses.

Researchers in the United Kingdom searched the Embase and Medline databases from 1966 to 2012 for studies reporting anti-Epstein-Barr virus (EBV) antibodies in sera from systemic lupus erythematosus (SLE) and control cases. Two researchers reviewed 200 titles and abstracts to identify studies eligible for inclusion. Detection of anti-EBV antibodies was calculated using Mantel-Haenszel ORs. A modified version of the Newcastle-Ottawa scale was used to conduct quality assessments.

Twenty-five case-control studies were deemed eligible. Median sample sizes were 60 for the SLE groups and 50 for the control cohorts. In assessing case quality, researchers said most studies reported acceptable selection criteria but recruitment procedures for cases and controls were described poorly.

Among patients with SLE, a statistically significant higher seroprevalence of anti-viral capsid antigen (VCA) immunoglobulin G (IgG; OR=2.08; 95% CI, 1.15-3.76) was reported, but not anti-EBV-nuclear antigen1 (EBNA1; OR=1.45; 95% CI, 0.7-2.98) when compared with control cohorts. In meta-analyses, significantly high ORs were reported for anti-early antigen (EA)/D IgG (OR=4.5; 95% CI, 3-11.06) and anti-VCA IgA (OR=5.05; 95% CI, 1.05-13.13). Anti-VCA analysis suggested asymmetry of the funnel plot and publication bias.

“These findings support the hypothesis that prior infection with EBV is important in the development of SLE, as indicated by a higher seroprevalence of anti-VCA IgG,” the researchers concluded. “They also suggest dysregulated (anti-EA/D, IgA) immune responses to EBV in the context of SLE.

“Further, larger studies with more precise matching and descriptions of recruitment and measurement … addressing the questions of both precedence and the possibility of spurious results from abnormal humoral immune reactivity secondary to the disease, are needed to establish the relationship between infection with EBV and SLE.”

Disclosure: The researchers report no relevant financial disclosures.

Epstein-Barr virus infection contributed to the development of systemic lupus erythematosus, according to a recent systematic review and meta-analyses.

Researchers in the United Kingdom searched the Embase and Medline databases from 1966 to 2012 for studies reporting anti-Epstein-Barr virus (EBV) antibodies in sera from systemic lupus erythematosus (SLE) and control cases. Two researchers reviewed 200 titles and abstracts to identify studies eligible for inclusion. Detection of anti-EBV antibodies was calculated using Mantel-Haenszel ORs. A modified version of the Newcastle-Ottawa scale was used to conduct quality assessments.

Twenty-five case-control studies were deemed eligible. Median sample sizes were 60 for the SLE groups and 50 for the control cohorts. In assessing case quality, researchers said most studies reported acceptable selection criteria but recruitment procedures for cases and controls were described poorly.

Among patients with SLE, a statistically significant higher seroprevalence of anti-viral capsid antigen (VCA) immunoglobulin G (IgG; OR=2.08; 95% CI, 1.15-3.76) was reported, but not anti-EBV-nuclear antigen1 (EBNA1; OR=1.45; 95% CI, 0.7-2.98) when compared with control cohorts. In meta-analyses, significantly high ORs were reported for anti-early antigen (EA)/D IgG (OR=4.5; 95% CI, 3-11.06) and anti-VCA IgA (OR=5.05; 95% CI, 1.05-13.13). Anti-VCA analysis suggested asymmetry of the funnel plot and publication bias.

“These findings support the hypothesis that prior infection with EBV is important in the development of SLE, as indicated by a higher seroprevalence of anti-VCA IgG,” the researchers concluded. “They also suggest dysregulated (anti-EA/D, IgA) immune responses to EBV in the context of SLE.

“Further, larger studies with more precise matching and descriptions of recruitment and measurement … addressing the questions of both precedence and the possibility of spurious results from abnormal humoral immune reactivity secondary to the disease, are needed to establish the relationship between infection with EBV and SLE.”

Disclosure: The researchers report no relevant financial disclosures.