Mehrsa Rashidpour,1Saman Hakimian,2,*
1. Bachelor student of Apadana University-Shiraz 2. M.sc student of pathogenic microbes Islamic Azad - University central tehran Branch
Introduction: Epstein–Barr virus (EBV) contributes to about 1.5% of all cases of human cancer worldwide, and viral genes are expressed in the malignant cells. EBV also very efficiently causes the proliferation of infected human B lymphocytes. The functions of the viral proteins and small RNAs that may contribute to EBV-associated cancers are becoming increasingly clear, and a broader understanding of the sequence variation of the virus genome has helped to interpret their roles. The improved understanding of the mechanisms of these cancers means that there are great opportunities for the early diagnosis of treatable stages of EBV-associated cancers and the use of immunotherapy to target EBV-infected cells or overcome immune evasion. There is also scope for preventing disease by immunization and for developing therapeutic agents that target the EBV gene products expressed in the cancers.
Epstein-Barr virus (EBV)-positive mucocutaneous ulcers (EBVMCUs) were first described as a lymphoproliferative disorder in 2010.
Methods: Certain EBV-associated diseases, such as Burkitt lymphomas and nasopharyngeal carcinomas, are endemic and exhibit biased geographic distribution worldwide. Recent advances in deep sequencing technology enabled high-throughput sequencing of the EBV genome from clinical samples. Rapid cloning and sequencing of cancer-derived EBV genomes, followed by reconstitution of infectious virus, have also become possible. These developments have revealed that various EBV strains are differentially distributed throughout the world, and that the behavior of cancer-derived EBV strains is different from that of the prototype EBV strain of non-cancerous origin.
Epstein–Barr virus (EBV)-associated gastric cancer (EBVaGC) is regarded as the most prevalent malignant tumor triggered by EBV infection
In the latest research on EBV, it was found that this virus could encode miRNAs. Mechanistically, EBV-encoded miRNAs are involved in carcinogenesis and the progression of EBV-associated malignancies.
Results: Epstein-Barr virus (EBV) is a ubiquitous herpes virus that infects the majority of the population worldwide. The virus can establish a lifelong latent infection in host B-lymphocytes. In the setting of immunocompromise as is the case post transplantation, the virus can reactivate and cause one of the deadliest complications post hematopoietic stem cell transplantation (HSCT), post-lymphoproliferative disease (PTLD), the incidence of which has been increasing. Multiple risk factors have been associated with the onset of PTLD such as age, reduced intensity conditioning, EBV serology mismatch and cytomegalovirus (CMV) reactivation. The rarity of clinical trials involving PTLD and the lack of approved treatment modalities renders the management of PTLD challenging. While the first-line treatment involves weekly administration of rituximab, there is no consensus when treating rituximab-refractory PTLD. There is a handful of clinical trials that investigate the role of EBV-specific cytotoxic T-lymphocytes (CTLs) and novel agents, such as bortezomib, lenalidomide, everolimus, panobinostat, and brentuximab. This article aims to explore the entity of EBV-PTLD in HSCT recipients, expanding on clinical presentation, risk factors, modes of monitoring and treatment, and so highlighting the gaps in knowledge that are needed in order to build a treatment paradigm suitable for all patients at risk.
Conclusion: Most of the cases show monoclonal TCR rearrangements . Moreover, chromosomal aberrations have been reported in some cases and turned out to be associated with the poorest outcomes . As STCLC have many clinicopatholgical features overlapping with EBV-associated HLH, the identification of karyotypic abnormalities should therefore be helpful to distinguish these two entities.
Many studies to date have demonstrated an association between SLE and EBV infection. A higher EBV seroconversion rate was observed in both pediatric and adult SLE patients compared to healthy controls .
Mouse models, either humanized or MHV infection of lupus prone mice, may be an alternate approach to decipher the role of EBV. CD34+ hematopoietic stem cells generated in vitro from induced pluripotent stem cells (iPSC), which are EBV negative, to reconstitute BLT mice described by Melkus et al. can overcome the effects of prior exposure to EBV in patient cells. The use of iPSC also allows for introducing (or reverting) specific mutations to further clarify the gene/environment interactions, and determining immune dysregulation immediately following EBV infection.