Multiple sclerosis (MS) is a chronic immune-mediated disorder of the central nervous system (CNS) with multiple genetic and environmental risk factors. Long non-coding RNAs (lncRNAs) have been recently reported to participate in the regulation of immune responses. Consequently, aberrant expression of lncRNAs has been suggested as an underlying cause of MS. In the present study, we evaluated the expression of three lncRNAs with putative roles in the regulation of immune response, namely TNF-α and heterogeneous nuclear ribonucleoprotein L (THRIL), Fas cell surface death receptor- antisense 1 (FAS-AS1), and plasmacytoma variant translocation 1 (PVT1) in circulating blood cells of 50 Iranian relapsing-remitting multiple sclerosis (RRMS) patients compared with healthy subjects by means of quantitative real-time polymerase chain reaction (PCR). We detected a significant downregulation of PVT1 and FAS-AS1 expressions in RRMS patients while a significant upregulation of THRIL in patients compared with controls (P < 0.001). Correlation analyses between lncRNA expression levels and clinical data of MS patients revealed no significant correlation between lncRNAs expression levels and Expanded Disability Status Scale (EDSS), a moderate correlation between PVT1 expression levels and duration of the disorder and no significant correlation between lncRNAs expression levels and age at onset. In addition, we demonstrated correlations between the expression levels of PVT1 and THRIL as well as expression levels of THRIL and FAS-AS1 in RRMS patients. In brief, we have demonstrated dysregulation of three lncRNAs in MS patients. Further studies are needed to explore the exact mechanisms by which these lncRNAs participate in regulation of immune responses.

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The results of the current research partially solved the puzzling question of complex interplay between environmental factors and MS disease in this part of Iran. Incorporating these factors enables more powerful and accurate detection of novel risk factors with diagnostic and prognostic methods.

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Autism is a neurodevelopmental disease that manifested by a wide range of behavioral disorders. Although the etiology of autism is remained unknown but it is suggested that ASD have a complex etiology, including genetic and environmental factors, which may explain the observed different behavioral disorders in these patients. One of the proposed reasons for autism is viral infection in the early stages of development. The mechanism by which viral infection could lead to autism is still unclear.Previous studiesemphasized on the role of family membersof Herpesviruses in autism susceptibility. In this study, anti-Cytomegalovirus (CMV) and anti-Epstein-Barr virus (EBV) antibodies in the serum of 45 children with autism and 45 healthy individuals were evaluated. Serum samples were isolated from 5 ml blood of the patients and controls. Sandwich ELISA was used to quantitatively measure antibodies against the mentioned viruses. Results analyzed by SPSS software showed an increased amount of anti-CMV IgG and IgM antibodies in the blood of patients with Autism but not statistically significant (P< 0.05). The anti-EBV IgM antibody in the blood of patients with Autism was not only increased but also statistically significant (P< 0.05), however, the IgG level against EBV in the serum of ASD patients showed no significant difference in comparison to healthy controls. So it can be said that although the mechanisms of viral infection in autism is unknown, but probably EBV infection is associated with an increased risk of autism.

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