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

Lupus ◽  
2021 ◽  
pp. 096120332110103
Author(s):  
Anna Truszewska ◽  
Agnieszka Wirkowska ◽  
Kamila Gala ◽  
Piotr Truszewski ◽  
Łucja Krzemień-Ojak ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Renal Damage ◽  
Healthy Individuals ◽  
Pcr Assay ◽  
Barr Virus ◽  
Fragmentation Index ◽  
Epstein Barr

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 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 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, R2 = 0.13), and the correlation was even more pronounced in CKD (+) patients (P < 0.001, R2 = 0.20). 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.

Epstein–Barr virus, cytomegalovirus and BK polyomavirus burden in juvenile systemic lupus erythematosus: correlation with clinical and laboratory indices of disease activity

Lupus ◽  
2020 ◽  
Vol 29 (10) ◽  
pp. 1263-1269
Author(s):  
Deniz Aygun ◽  
Mert Ahmet Kuskucu ◽  
Sezgin Sahin ◽  
Amra Adrovic ◽  
Kenan Barut ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Healthy Controls ◽  
Healthy Individuals ◽  
Systemic Lupus ◽  
Barr Virus ◽  
Bk Polyomavirus ◽  
Ebv Dna ◽  
Epstein Barr

Objectives Clinical and laboratory investigations have revealed that Epstein–Barr virus (EBV) is involved in altered immunological response of systemic lupus erythematosus (SLE). Higher seroprevalence rates of anti-EBV antibodies and increased viral load are demonstrated in adult SLE patients. The prevalence of BK polyomavirus (BKV) reactivation is also suggested to be higher in SLE. Herein, we aimed to evaluate the immune response of children with SLE to EBV antigens in addition to EBV and BKV DNA. We also tried to evaluate whether these serological results differ from another connective tissue disease – juvenile systemic sclerosis (jSS) – and healthy individuals. Methods Serum levels of EBV early antigen diffuse (EA-D) IgG, EBV nuclear antigen-1 IgG, EBV viral capsid antigen (VCA), cytomegalovirus (CMV) IgG, EBV DNA, CMV DNA and urinary BKV DNA were evaluated in healthy controls and in patients with a diagnosis of juvenile SLE (jSLE) and jSS. Results A total of 70 jSLE patients, 14 jSS patients and 44 sex-matched healthy individuals were involved in the study. EBV VCA was positive in 84.2% of jSLE patients, 85.7% of jSS patients and 36.3% of healthy controls. EBV EA-D IgG positivity was significantly higher in jSLE patients compared to jSS patients and healthy controls (20% vs. 7.1% and 0%, p = 0.005). EBV VCA positivity was associated with malar rash and immunological disorder, but there was no statistical significance in other antibody positivity in terms of clinical and haemogram findings and autoantibody positivity. CMV DNA positivity was present in only 2.8% of jSLE patients. None of the jSS patients or the healthy controls had CMV DNA positivity. EBV DNA and BKV DNA were also negative in all three groups. Conclusion The results of our study assume a relationship between SLE and EBV, but we could not demonstrate an association between CMV and BKV. The negative DNA results in contrast to serological positivity can be interpreted as an altered and impaired immune system and increased viral susceptibility. These results suggest that EBV contributes to disease continuity, even if it does not directly cause development.

scholarly journals Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 277 ◽  
Author(s):  
Marco Quaglia ◽  
Guido Merlotti ◽  
Marco De Andrea ◽  
Cinzia Borgogna ◽  
Vincenzo Cantaluppi
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune Response ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Viral Infections ◽  
Systemic Lupus ◽  
Barr Virus ◽  
Epstein Barr ◽  
The Impact

A causal link between viral infections and autoimmunity has been studied for a long time and the role of some viruses in the induction or exacerbation of systemic lupus erythematosus (SLE) in genetically predisposed patients has been proved. The strength of the association between different viral agents and SLE is variable. Epstein–Barr virus (EBV), parvovirus B19 (B19V), and human endogenous retroviruses (HERVs) are involved in SLE pathogenesis, whereas other viruses such as Cytomegalovirus (CMV) probably play a less prominent role. However, the mechanisms of viral–host interactions and the impact of viruses on disease course have yet to be elucidated. In addition to classical mechanisms of viral-triggered autoimmunity, such as molecular mimicry and epitope spreading, there has been a growing appreciation of the role of direct activation of innate response by viral nucleic acids and epigenetic modulation of interferon-related immune response. The latter is especially important for HERVs, which may represent the molecular link between environmental triggers and critical immune genes. Virus-specific proteins modulating interaction with the host immune system have been characterized especially for Epstein–Barr virus and explain immune evasion, persistent infection and self-reactive B-cell “immortalization”. Knowledge has also been expanding on key viral proteins of B19-V and CMV and their possible association with specific phenotypes such as antiphospholipid syndrome. This progress may pave the way to new therapeutic perspectives, including the use of known or new antiviral drugs, postviral immune response modulation and innate immunity inhibition. We herein describe the state-of-the-art knowledge on the role of viral infections in SLE, with a focus on their mechanisms of action and potential therapeutic targets.

scholarly journals EBV-1 and HCMV in aggressive periodontitis in Brazilian patients

2007 ◽  
Vol 21 (4) ◽  
pp. 336-341 ◽  
Author(s):  
Soraia Almeida Watanabe ◽  
Jeane de Fátima Correia-Silva ◽  
Martinho Campolina Rebello Horta ◽  
José Eustáquio da Costa ◽  
Ricardo Santiago Gomez
Keyword(s):  
Epstein Barr Virus ◽  
Positive Association ◽  
Aggressive Periodontitis ◽  
Periodontal Pocket ◽  
Pcr Assay ◽  
Barr Virus ◽  
Epstein Barr ◽  
Crevicular Fluid

The purpose of the present investigation was to compare the presence of Epstein-Barr virus type 1 (EBV-1) and of Human Cytomegalovirus (HCMV) in crevicular fluid samples from deep and shallow periodontal pocket sites of Brazilian patients with aggressive periodontitis. A total of 30 systemically healthy patients with aggressive periodontitis participated in the study. Paper points were inserted into 2 gingivitis sites (< 3 mm) and into 2 periodontitis sites (> 5 mm) in each patient. PCR assay was used to identify genomic copies of HCMV and EBV-1. Twenty-three patients (77%) were positive for EBV-1, while only 2 patients (6%) were positive for HCMV. The McNemar test revealed a positive association between EBV-1 and periodontal lesions (p = 0.043). Thirty-four (57%) out of 60 periodontitis sites were positive for EBV-1, whereas 18 (30%) gingivitis sites were positive (p = 0.01). Only two sites (6.7%) were positive for HCMV. No positive association was found between HCMV and periodontitis or gingivitis (p = 0.479). The elevated occurrence of EBV-1 DNA in periodontal pockets of patients with aggressive periodontitis supports a possible periodontopathic role of this virus.

scholarly journals Epstein–Barr Virus in Salivary Samples from Systemic Lupus Erythematosus Patients with Oral Lesions

2021 ◽  
Vol 10 (21) ◽  
pp. 4995
Author(s):  
Alessio Buonavoglia ◽  
Patrizia Leone ◽  
Marcella Prete ◽  
Antonio Giovanni Solimando ◽  
Chiara Guastadisegno ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Oral Lesions ◽  
Systemic Lupus ◽  
Real Time Quantitative Pcr ◽  
Barr Virus ◽  
Ebv Dna ◽  
Epstein Barr

In order to investigate the possible role of Epstein–Barr virus (EBV) in systemic lupus erythematosus (SLE) and its associated oral lesions, a pilot case–control study was performed. A total of 31 patients (18 females and 13 males) were enrolled in the study and divided into two groups: group A included 16 patients with diagnosis of SLE and group B included 15 healthy individuals. Salivary swab samples were collected and subjected to molecular screening by real-time quantitative PCR (qPCR) for the detection of EBV DNA. EBV DNA was significantly detected in 8/16 (50%) SLE patients and in 5/7 (71.4%) subjects with SLE-associated oral lesions. Since EBV is one of the most common viruses in the human population, it is difficult to understand if it is the causative agent of SLE or, vice versa, if SLE is able to trigger the reactivation of EBV. This study highlights a significant association between the presence of EBV and both SLE and SLE-related oral lesions and provides rationale for further investigation into the role of EBV in SLE pathogenesis.

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