A new groundbreaking study has recently identified the link between the long-standing mystery in autoimmune disease: Epstein-Barr Virus (EBV) and how it contributes towards the development of systemic lupus erythematosus (SLE). The study found that EBV infects a small subset of autoreactive B-cells, and reprograms them into antigen-presenting cells (APCs)that mistakenly respond to the body’s own tissues, fueling the development of lupus. EBV has been associated with diseases like Long COVID, multiple sclerosis, and SLE in the past. However, the “why” behind this link has not been identified.
Researchers used a novel single-cell RNA sequencing technique to identify EBV infected b cells, along with chromatin and polymerase II occupancy analyses, to identify EBV-infected B cells. It was found that these cells were significantly different than their uninfected counterparts. EBV-infected B cells exhibited features associated with antigen presentation such as the up-regulation of genes like ZEB2 and TBX21 and expression of CD27+CD21-/low memory-B phenotype, which is a critical piece in triggering immune responses. This programming seemed likely to be directly driven by the EBV protein EBNA2.
EBV may be a contributor to the initiation and development of the immunity activity seen in lupus. Early results like this pave the way towards understanding the connection and can offer new insight into how targeting EBV-infected B cells or the ERBNA2 protein could treat lupus or minimize its effect. However, more research is needed. Learn more about SLE.
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