Epstein Barr Virus and Autoimmune Responses in Systemic Lupus Erythematosus

Jog, Neelakshi R.; James, Judith A.

doi:10.3389/fimmu.2020.623944

Cited by 84 publications

(64 citation statements)

References 93 publications

(88 reference statements)

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“…Significantly high levels of vIL-10 have been observed in SLE patients' plasma compared to unaffected controls, supporting the hypothesis of EBV reactivation in SLE patients [18]. Furthermore, vIL-10 levels in [18] correlated with levels of IgA antibodies specific to the EBV viral capsid antigen, which is an indirect measure of viral reactivation. In SLE patients, the anti-inflammatory effects of hIL-10 are overcome by vIL-10, resulting in an increase in inflammatory gene expression and an exacerbation of autoimmune responses [18].…”

Section: Introductionsupporting

confidence: 54%

“…Immune impairment can trigger EBV reactivation with a new lithic phase and production of infectious virions. This process initiates a new round of epithelial infection in the tonsils and viral shedding in the saliva [18].…”

Section: Introductionmentioning

confidence: 99%

“…Zta induces the transcription of viral and cellular genes and increases the production of autoantibodies against dsDNA (anti-dsDNA) [20]. Moreover, EBV encodes several viral homologues of human proteins, such as EBV IL-10 (vIL-10), which is homologous to the human IL-10 (hIL-10); it is produced during the lytic phase of the virus and encoded by the viral BCRF1 gene [18,20]. It is an immunosuppressive cytokine that inhibits IFN-γ and TNF-α production and CD8+ cytotoxic T cell and MHC-I expression in favoring immune surveillance inhibition [18,21].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, EBV encodes several viral homologues of human proteins, such as EBV IL-10 (vIL-10), which is homologous to the human IL-10 (hIL-10); it is produced during the lytic phase of the virus and encoded by the viral BCRF1 gene [18,20]. It is an immunosuppressive cytokine that inhibits IFN-γ and TNF-α production and CD8+ cytotoxic T cell and MHC-I expression in favoring immune surveillance inhibition [18,21]. Significantly high levels of vIL-10 have been observed in SLE patients' plasma compared to unaffected controls, supporting the hypothesis of EBV reactivation in SLE patients [18].…”

Section: Introductionmentioning

confidence: 99%

“…It is an immunosuppressive cytokine that inhibits IFN-γ and TNF-α production and CD8+ cytotoxic T cell and MHC-I expression in favoring immune surveillance inhibition [18,21]. Significantly high levels of vIL-10 have been observed in SLE patients' plasma compared to unaffected controls, supporting the hypothesis of EBV reactivation in SLE patients [18]. Furthermore, vIL-10 levels in [18] correlated with levels of IgA antibodies specific to the EBV viral capsid antigen, which is an indirect measure of viral reactivation.…”

Section: Introductionmentioning

confidence: 99%

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

Buonavoglia

Leone

Prete

et al. 2021

JCM

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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.

show abstract

Section: Introductionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

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

Buonavoglia

Leone

Prete

et al. 2021

JCM

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Unique Interplay Between Antinuclear Antibodies and Nuclear Molecules in the Pathogenesis of Systemic Lupus Erythematosus

Pisetsky

2024

Arthritis & Rheumatology

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Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease that primarily affects young women and causes a wide range of inflammatory manifestations. The hallmark of SLE is the production of antibodies to components of the cell nucleus (antinuclear antibodies or ANAs). These antibodies can bind to DNA, RNA and protein complexes with nucleic acids. Among ANAs, antibodies to DNA (anti‐DNA) are markers for classification and disease activity, waxing and waning in many patients. In the blood, anti‐DNA antibodies can bind DNA to form immune complexes with two distinct roles in pathogenesis: renal deposition to provoke nephritis and stimulation of cytokine production following uptake into innate immune cells and interaction with internal nucleic acid sensors. These sensors are part of an internal host defense system in the cell cytoplasm that can respond to DNA from infecting organisms; during cell stress, DNA from nuclear and mitochondrial sources can also trigger these sensors. The formation of immune complexes requires a source of extracellular DNA in an immunologically accessible form. As shown in in vivo and in vitro systems, extracellular DNA can emerge from dead and dying cells in both a free and particulate form. Neutrophils undergoing the process of NETosis can release DNA in mesh‐like structures called NETs (neutrophil extracellular traps). In SLE, therefore, the combination of ANAs and immunologically active DNA can create new structures which can promote inflammation throughout the body as well as drive organ inflammation and damage.

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Generalized lymphadenopathy in the presence of acute Epstein–Barr virus infection as the initial manifestation of systemic lupus erythematous: A case report

Jazi,

Faraji,

Aghaei

et al. 2024

Clinical Case Reports

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Key Clinical MessageClinicians should carefully consider generalized lymphadenopathy, particularly post viral infections, as one of the possible systemic lupus erythematous (SLE) first signs regarding unusual joint involvements such as sacroiliitis. Late diagnosis of this autoimmune inflammatory disease, could lead to irreversible morbidity and higher mortality.AbstractLymphadenopathy could represent various etiologies, including infections, malignancies, and rheumatologic diseases. SLE is known as the great mimicker which could be presented with different first manifestations. We report a 42‐year‐old woman in the acute phase of Epstein–Barr infection, admitted with polyarticular peripheral arthritis, sacroiliitis, and generalized lymphadenopathy. She had no similar history or taken unpasteurized dairy. Nodes were soft, mobile, and tender without skin change on top. During the process, she was diagnosed with SLE and discharged with prednisolone 30 mg/day and hydroxychloroquine 400 mg/day. After 2 weeks of follow‐up, all lymphadenopathy and symptoms were diminished. This case underscores the thousand faces innate of SLE. Clinical awareness would lead to an accurate diagnosis and early intervention.

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Epstein Barr Virus and Autoimmune Responses in Systemic Lupus Erythematosus

Cited by 84 publications

References 93 publications

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

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

Unique Interplay Between Antinuclear Antibodies and Nuclear Molecules in the Pathogenesis of Systemic Lupus Erythematosus

Generalized lymphadenopathy in the presence of acute Epstein–Barr virus infection as the initial manifestation of systemic lupus erythematous: A case report

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