Abstract

Epstein-Barr virus (EBV) is a ubiquitous virus belonging to the human γ-herpes virus subfamily. After primary infection, EBV maintains a life-long latent infection. A major concern is that EBV can cause a diverse range of neoplasms and autoimmune diseases. In addition, patients undergoing hematopoietic stem cell transplantation or solid organ transplantation can experience post-transplant lymphoproliferative disorders (PTLDs) due to dysfunction or suppression of host’s immune system, or uncontrolled proliferation of EBV-infected cells. In recent years, the number of EBV-associated PTLD cases has increased. This review focuses on the current understandings of EBV-associated PTLD pathogenesis, as well as the risk factors and clinical outcomes for patients after allogeneic stem cell transplantation.

Highlights

  • Epstein-Barr virus (EBV) infects more than 90% of the adult population worldwide at some point in their lives, usually with no ill effects [1]

  • EBV has been identified as the cause of several human cancers, including nasopharyngeal carcinoma and Hodgkin’s lymphoma; it is responsible for post-transplant lymphoproliferative disorder (PTLD) [3]

  • The 2017 revised 4th edition of the World Health Organization classification recognizes four different entities: non-destructive PTLD characterized histologically by a lack of architectural effacement, polymorphic PTLD characterized by a full spectrum of lymphoid maturation but not satisfying the criteria for lymphoma, monomorphic PTLD (B-cell neoplasms and T/NK-cell neoplasms which are classified in more detail according to the historical characteristics of the lymphoma they most resemble), and classical Hodgkin lymphoma PTLD (Table 1)

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Summary

Introduction

Epstein-Barr virus (EBV) infects more than 90% of the adult population worldwide at some point in their lives, usually with no ill effects [1]. EBV was first identified in 1964 from a patient with Burkitt’s lymphoma, suggesting that EBV is a causative agent of human cancer [2]. EBV maintains a life-long latent infection of memory B-cells; the virus can cause a range of neoplasms attributable to dysregulated proliferation of EBV-infected B-cells due to dysfunction or suppression of the host immune system after transplantation. The most common histological subtype of monomorphic PTLD is diffuse large B-cell lymphoma, which accounts for ~60% of cases. Other subtypes such as Burkitt lymphoma, plasma cell neoplasms and T-cell lymphoma have been reported [6,7].

EBV Infection and Latent Status
EBV-Induced Oncogenesis
Hematopoietic Stem Cell Transplantation Setting
Genetic or Epigenetic Alternations
Epidemiology
Risk Factors
Factors after HSCT
Clinical
Hematoxylin andand eosin staining of PTLD tissue samples from the
Treatments
Propylaxis
Pre-Emptive Therapy
Rituximab
Chemotherapy
Adoptive Immunotherapy
Possible Future Therapy
Reduction of Immunosuppression
Other Strategy
Management for Rare Cases
Treatment Response Evaluation
Prognosis
Conclusions
Results
Full Text
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