Human herpesvirus infections and circulating microvesicles expressing galectin-3 binding protein in patients with systemic lupus erythematosus

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Objective. Circulating microvesicles (MVs) expressing the type 1 interferoninducible protein galectin-3 binding protein (G3BP) are potentially major sources of autoantigens in systemic lupus erythematosus (SLE). In this study, we explore if plasma concentrations of G3BP-expressing MVs correlate with signs of various active human herpesvirus (HHV) infections in SLE patients, suggesting a virus-induced mechanism for the generation of these vesicles. Methods. In 49 SLE patients, the plasma levels of immunoglobulin G (IgG) against cytomegalovirus (CMV) pp52, Epstein-Barr virus (EBV) early antigen diffuse (EA/D), and HHV6 p41 were measured by ELISAs and used as humoral markers of ongoing/recently active viral infection. MVs in plateletpoor plasma were quantified and characterised by flow cytometry, with regard to the binding of Annexin V (AnxV) and the expression of G3BP. Spearman's rho and the Wilcoxon rank-sum test were applied for associative evaluation of virus serology with MV subsets, and clinical and demographic data. Results. The CMV pp52-directed antibodies correlated positively with the high G3BP-expressing MVs; either low (rho=0.4, p-value=0.005) or high (rho=0.37, p-value=0.01) in AnxVexpression. Furthermore, these MV subsets were higher in individuals with high and low IgG levels against CMV pp52 and EBV EA/D, respectively, relative to subjects with low and high IgG levels against these HHV antigens. Importantly, none of the associations were explained by immunosuppressants or antimalarials. Conclusion. Ongoing/recently active CMV infection is associated with circulating MVs expressing G3BP in SLE patients, supporting a link between specific viral infections and potentially pathogenic MVs in SLE.

OriginalsprogEngelsk
TidsskriftClinical and Experimental Rheumatology
Vol/bind40
Udgave nummer1
Sider (fra-til)158-161
Antal sider4
ISSN0392-856X
DOI
StatusUdgivet - 2022

Bibliografisk note

Funding Information:
The authors thank Esin Djebir Güven and Dorte T. Olsen, Department of Au-toimmunology and Biomarkers, Statens Serum Institut, Copenhagen, Denmark for collecting blood samples. Moreover, we also thank Kirsten Beth Hansen for assistance on the flow cytometry analysis. Some of the included data were generated with financial support by the Danish Rheumatism Association.

Publisher Copyright:
© Copyright Clinical and Experimental Rheumatology 2022.

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