No abstract

Autoimmune diseases develop due to self-tolerance failure in recognizing self and non-self-antigens. Several factors play a role in inducing autoimmunity, including genetic and environmental elements. Several studies demonstrated the causative role of viruses; however, some studies showed the preventive effect of viruses in the development of autoimmunity. Neurological autoimmune diseases are classified based on the targets of autoantibodies, which target intracellular or extracellular antigens rather than neurons. Several theories have been hypothesized to explain the role of viruses in the pathogenesis of neuroinflammation and autoimmune diseases. This study reviewed the current data on the immunopathogenesis of viruses in autoimmunity of the nervous system.

Background: Rheumatoid arthritis (RA) is an autoimmune disease with an unknown etiology. Both genetic and environmental factors play important roles. This study aimed to investigate the possible associations between toll-like receptor 9 (TLR9) single nucleotide polymorphisms (SNPs) and the risk of RA or Epstein-Barr virus (EBV) infection, as well as the probable link between EBV infection, TLR9 gene variants, and risk of RA among Iranians.Method: 213 RA patients and 235 healthy individuals participated in this study. TLR9 SNPs rs187084 and rs352140 were evaluated using polymerase chain reaction-restriction fragment length polymorphism (RFLP-PCR) while EBV DNA was determined by real-time PCR.Results: The frequency of rs352140 CT and TT+CT genotypes was significantly higher in healthy individuals compared with RA patients (p=0.01 and p=0.02 respectively). Furthermore, TC/TC haplotype combination was more frequently seen in RA patients (p= 0.01). EBV infection was more frequently detected in RA patients compared to the controls (p=0.04). Moreover, a significantly higher frequency of the rs187084 C allele was observed in EBVneg infected healthy subjects, in particular in females (p=0.05 and p=0.04 respectively).Conclusion: EBV infection and TC/TC haplotype combination might act as a susceptibility factor for RA while rs352140 CT genotype and rs352140 CT+TT genotype combination might be protective. In addition, the rs187084 C allele might protect EBVneg infected subjects from developing RA.