Viral Infections and Systemic Lupus Erythematosus: Pathophysiological Roles of Parvovirus and Epstein-Barr Virus Infections

ElMelegy, Tarek T. H.; Omran, Safaa A.; Radwan, Amany H.; Herdan, Omar M.; Rashed, Hebatallah G.

doi:10.21608/jcmrp.2024.279792.1041

Viral Infections and Systemic Lupus Erythematosus: Pathophysiological Roles of Parvovirus and Epstein-Barr Virus Infections

Document Type : Original Article

Authors

¹ Department of Clinical Pathology, Faculty of Medicine, Assiut University, Assiut, Egypt.

² Department of Internal Medicine, Faculty of Medicine, Assiut University, Assiut, Egypt.

10.21608/jcmrp.2024.279792.1041

Abstract

Abstract:
Background: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune-mediated tissue damage affecting different organs. The pathogenesis of SLE is multifactorial and involves interaction between genetic and environmental factors, culminating in the breaking of immune self-tolerance. Viral infections such as parvovirus and Epstein–Barr virus can trigger or worsen SLE disease, stimulating the immune processes via different mechanisms.
Aim: This study was designed to investigate the possible role of parvovirus and Epstein–Barr virus in the pathogenesis of SLE and its relation to disease activity.
Patients and Methods: This study was conducted on 90 SLE female patients and 83 healthy controls. Disease activity was assessed according to the systemic lupus disease activity index (SLEDAI-2K) score. IgG antibodies against parvovirus and Epstein–Barr virus, blood parameters (hemoglobin, platelet count, and white blood cell count), serum albumin, kidney function parameters (urea, creatinine, 24-hour-urine protein, urine analysis), and immune parameters (C3, C4, and anti-dsDNA) were evaluated using appropriate methods.
Results: There was no statistically significant increase in IgG antibodies against parvovirus and Epstein–Barr virus infections in SLE patients compared to the control group. There was also no statistically significant difference between patients with positive and negative test results for IgG antibodies against parvovirus and Epstein–Barr virus infections regarding blood parameters, kidney function parameters, immune parameters, and SLE disease activity.
Conclusion: Parvovirus and Epstein–Barr virus infections have a similar frequency in SLE patients and controls. In addition, these infections did not have evident pathophysiological effects in SLE patients. More studies are required to confirm these findings.

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