EBV load is associated with cfDNA fragmentation and renal damage in SLE patients.


Journal

Lupus
ISSN: 1477-0962
Titre abrégé: Lupus
Pays: England
ID NLM: 9204265

Informations de publication

Date de publication:
Jul 2021
Historique:
pubmed: 20 4 2021
medline: 16 12 2021
entrez: 19 4 2021
Statut: ppublish

Résumé

For long Epstein-Barr virus (EBV) has been suspected to be involved in the pathogenesis of systemic lupus erythematosus (SLE). The aim of this study was to verify the association between EBV, cell-free DNA (cfDNA) and kidney disease in SLE. Blood samples were obtained from 43 SLE patients and 50 healthy individuals. EBV load was measured via real-time PCR assay. Sizing and quantification of plasma cfDNA was performed on Bioanalyzer. We proposed that the uniformity of cfDNA fragmentation can be described using cfDNA fragmentation index. SLE patients with chronic kidney disease (CKD +) had higher EBV load compared to CKD(-) patients (P = 0.042). Patients with high cfDNA level had higher EBV load (P = 0.041) and higher cfDNA fragmentation index (P < 0.001) compared to patients with low cfDNA level. Among patients with high cfDNA level, EBV load was higher in CKD(+) group compared to CKD(-) group (P = 0.035). EBV load was positively correlated with the fragmentation index in all SLE patients (P = 0.028, R We showed that EBV load was associated with non-uniform cfDNA fragmentation, higher cfDNA levels, and kidney disease in SLE patients. Although the causality of this relationship could not be determined with the current study, it brings rationale for further investigations on the role of EBV and cfDNA interplay in SLE pathogenesis.

Sections du résumé

BACKGROUND BACKGROUND
For long Epstein-Barr virus (EBV) has been suspected to be involved in the pathogenesis of systemic lupus erythematosus (SLE). The aim of this study was to verify the association between EBV, cell-free DNA (cfDNA) and kidney disease in SLE.
METHODS METHODS
Blood samples were obtained from 43 SLE patients and 50 healthy individuals. EBV load was measured via real-time PCR assay. Sizing and quantification of plasma cfDNA was performed on Bioanalyzer. We proposed that the uniformity of cfDNA fragmentation can be described using cfDNA fragmentation index.
RESULTS RESULTS
SLE patients with chronic kidney disease (CKD +) had higher EBV load compared to CKD(-) patients (P = 0.042). Patients with high cfDNA level had higher EBV load (P = 0.041) and higher cfDNA fragmentation index (P < 0.001) compared to patients with low cfDNA level. Among patients with high cfDNA level, EBV load was higher in CKD(+) group compared to CKD(-) group (P = 0.035). EBV load was positively correlated with the fragmentation index in all SLE patients (P = 0.028, R
CONCLUSIONS CONCLUSIONS
We showed that EBV load was associated with non-uniform cfDNA fragmentation, higher cfDNA levels, and kidney disease in SLE patients. Although the causality of this relationship could not be determined with the current study, it brings rationale for further investigations on the role of EBV and cfDNA interplay in SLE pathogenesis.

Identifiants

pubmed: 33866897
doi: 10.1177/09612033211010339
doi:

Substances chimiques

Cell-Free Nucleic Acids 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1214-1225

Auteurs

Anna Truszewska (A)

Department of Immunology, Transplantology and Internal Diseases, Medical University of Warsaw, Warsaw, Poland.
Postgraduate School of Molecular Medicine, Medical University of Warsaw, Warsaw, Poland.

Agnieszka Wirkowska (A)

Department of Immunology, Transplantology and Internal Diseases, Medical University of Warsaw, Warsaw, Poland.

Kamila Gala (K)

Department of Immunology, Transplantology and Internal Diseases, Medical University of Warsaw, Warsaw, Poland.

Piotr Truszewski (P)

Department of Orthopedics and Traumatology of Musculoskeletal System, Baby Jesus Clinical Hospital, Warsaw, Poland.

Łucja Krzemień-Ojak (Ł)

Laboratory of the Molecular Biology of Cancer, Centre of New Technologies, Warsaw, Poland.

Krzysztof Mucha (K)

Department of Immunology, Transplantology and Internal Diseases, Medical University of Warsaw, Warsaw, Poland.
Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warszaw, Poland.

Leszek Pączek (L)

Department of Immunology, Transplantology and Internal Diseases, Medical University of Warsaw, Warsaw, Poland.
Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warszaw, Poland.

Bartosz Foroncewicz (B)

Department of Immunology, Transplantology and Internal Diseases, Medical University of Warsaw, Warsaw, Poland.

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