EBNA2

AcronymDefinition
EBNA2Epstein-Barr Nuclear Antigen 2
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The Cincinnati Children's team suspects that the EBNA2 transcription factor from EBV is helping change how infected B cells operate, and how the body responds to those infected cells.
The new paper shows that seven seemingly unrelated disease states actually share a common set of abnormal transcription factors, each affected by the EBNA2 protein from the Epstein-Barr virus.
In the current study, the researchers found that EBNA2 and its related transcription factors activate some of the human genes associated with the risk for lupus and several other autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, juvenile idiopathic arthritis and celiac disease.
Sifting through and comparing a large collection of genetic and protein data from healthy individuals and those with autoimmune diseases, the team used RELI to identify regulatory regions in genes associated with the risk of developing lupus that also bound EBNA2 and its related transcription factors.
They are variably positive for EBER, LMP1, EBV latent membrane protein 2 (LMP2), EBV nuclear antigen 1 (EBNA1), and EBNA2 and are commonly associated with type II or type III EBV latency patterns [4].
Although a full panel of EBV-related proteins and nuclear antigens were not analyzed, her lymphoma cells were positive for LMP1 and EBNA2. Thus, it is likely that the patient's EBV status was in latency type III, which usually indicates impaired immune functions and portends aggressive clinical behaviors [4, 6].
EBV was detected by nonisotopic in situ hybridization and PCR (Bam HI-F, EBV nuclear antigen 2 (EBNA2), and latent membrane protein 1 (LMP-1) regions).
In our casuistic we found a predominance of type 1 EBNA2 virus among the 44 samples studied, corresponding to 75.0% of the total.
It is classified as latency type I because the expressed latent genes are restricted to BARF0, EBERs, EBNA1, and LMP2A, excluding EBNA2 or LMP1 which are essential for its transforming ability [107-109].
Latent proteins which promote B cell immortalization include EBNA-1, EBNA2, EBNA-3A, EBNA-3C, EBNA-LP, and LMP-1.
EBNA2 is an important transcription factor during latency as it controls the expression of all other latent viral genes [36].
These mimic external growth signals (LMP1 and LMP2) or directly regulate gene expression (EBNA2, EBNA3c), thereby driving the infected cell into proliferation [7].