Affiliations: [a] Virology Department, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran | [b] Molecular Biology Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran | [c] Autoimmune Diseases Research Center, Kashan University of Medical Sciences, Kashan, Iran | [d] Students’ Scientific Research Center (SSRC), Tehran University of Medical Sciences, Tehran, Iran | [e] Universal Scientific Education and Research Network (USERN), Tehran, Iran | [f] Department of Microbiology, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran
Correspondence:
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Corresponding author: Ahmad Piroozmand, Department of Microbiology, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran. Tel.: +98 913 2623523; Fax: +98 31 55541114; E-mail: [email protected].
Abstract: BACKGROUND: Considerable evidence supports that SLE could be related to apoptotic cells and EBV infection. OBJECTIVE: The aim of this study was to identify the transcriptional signature of EBV infection in SLE patients for survey of the molecular apoptosis signaling pathways. METHODS: The PBMCs gene expression profiles of healthy control and SLE patients were obtained from GEO. Functional annotation and signaling pathway enrichment were carried out using DAVID, KEGG. To validate bioinformatics analysis the changes in genes expression of some of obtained genes, Real time PCR was performed on PBMCs from 28 SLE patients and 18 controls. RESULTS: We found that mean viral load was 6013 ± 390.1 copy/μg DNA from PBMCs in all patients. QRT-PCR results showed that the expression of the DUSP1 and LAMP3 genes which had most changes in the logFC among 4 candidate genes, increased significantly in comparison with control. The consistent expression of LMP2 as viral latency gene involve in apoptosis signaling pathways was detected in SLE patients with EBV viral load and some controls. CONCLUSIONS: The study indicated that some cellular genes may have an important role in pathogenesis of SLE through apoptosis signaling pathways. Beside, EBV infection as an environmental risk factor for SLE may affect the dysfunction of apoptosis.
