Abstract
IntroductionEpstein-Barr virus (EBV)-associated tumors show different expression patterns of latency genes. Since in breast carcinoma this pattern is not yet fully described, our aim was to characterize EBV latency pattern in our EBV positive breast carcinoma series.MethodsThe study was conducted on 71 biopsies of breast carcinoma and in 48 non-neoplastic breast controls. EBNA1, LMP2A and LMP1 expression was assessed by immunohistochemistry with monoclonal antibodies, while viral genomic DNA and EBERs RNA transcripts expression was performed by in situ hybridization. EBV presence was confirmed by PCR.ResultsEBV genomic DNA and EBNA1 expression were detected in 31% (22/71) of patients specifically restricted to tumor epithelial cells in breast carcinoma while all breast control samples were negative for both viral DNA and EBNA1 protein. LMP2A was detected in 73% of EBNA1 positive cases, none of which expressed either LMP1 protein or EBERs transcripts.ConclusionsThese findings suggest that EBV expression pattern in the studied biopsies could be different from those previously observed in breast carcinoma cell lines and lead us to suggest a new, EBNA1, LMP2A positive and LMP1 and EBERs negative latency profile in breast carcinoma in our population.
Highlights
Epstein-Barr virus (EBV)-associated tumors show different expression patterns of latency genes
Epstein-Barr virus (EBV) is a ubiquitous human c-herpes virus that has been linked to a variety of lymphoid and epithelial malignancies, such as Burkitt (BL), Hodgkin (HL) and NK/T lymphomas, nasopharyngeal (NPC) and gastric carcinoma (GC).[1]
To discard the possibility that the positive signal was given by EBV infected infiltrating B-cells within the homogenized tissue, all samples were assayed for viral DNA genome by means of BamH1W DNA ISH and the results matched the 22 EBV EBERs PCR status for all the 71 cases
Summary
Epstein-Barr virus (EBV)-associated tumors show different expression patterns of latency genes. All herpes viruses display two phases in their infective cycle that together describe persistent infection; these are latency and lytic replication.[3] In EBV-associated tumors, the virus establishes a latent infection, which is characterized by the limited expression of a subset of viral latent genes. Latency II pattern express the EBERs, BARTs transcripts, EBNA1 protein and the latent membrane proteins (LMP1, LMP2A and LMP2B), and is associated to HL and NPC. While B cells have the potential to support any of these three types of latent infection, non-B cells generally display either a Latency I or Latency II type of infection.[6]
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