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An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection
Published on: March 30, 2018
Natural killer cell-type body cavity lymphoma following chronic active Epstein-Barr virus infection
Masao Ogata1, Tomoyuki Imamura, Syunji Mizunoe
1Second Department of Internal Medicine, Oita Medical University, Hasama-machi, Oita, Japan. mogata@oita-med.ac.jp
Insights
A rare case of natural killer cell lymphoma developed after chronic active Epstein-Barr virus (CAEBV) infection. This HHV-8 negative lymphoma responded well to combination chemotherapy.
Area of Science:
- Oncology
- Virology
- Immunology
Background:
- Chronic active Epstein-Barr virus (CAEBV) infection is a rare condition.
- Body cavity lymphoma (BCL) is an uncommon non-Hodgkin lymphoma.
Observation:
- A 69-year-old female presented with persistent fever and was diagnosed with CAEBV infection.
- She subsequently developed natural killer (NK) cell-type BCL.
- Lymphocytes in pleural effusion were abnormal (CD2+, CD7+, CD30+, CD56+, CD3-, CD4-).
Findings:
- Clonal proliferation of EBV-infected cells was confirmed in pleural effusion.
- T cell receptor gene rearrangement was not detected.
- Human herpesvirus type-8 (HHV-8) DNA was absent.
- High EBV DNA load in plasma confirmed CAEBV infection, despite normal antibody titers.
Implications:
- This case highlights a unique presentation of lymphoma following CAEBV infection.
- It demonstrates the development of HHV-8-negative BCL.
- Combination chemotherapy proved effective for this specific lymphoma type.
Abstract:
We describe a 69-year-old female who developed natural killer cell-type body cavity lymphoma following chronic active Epstein-Barr virus (CAEBV) infection. Examination of the patient's pleural effusion revealed large abnormal lymphocytes, which were CD2(+), CD7(+), CD30(+), CD56(+), CD3(-), and CD4(-). No rearrangement of T cell receptor genes was detected. Clonal proliferation of Epstein-Barr virus (EBV)-infected cells in pleural effusion was demonstrated by Southern blot hybridization analysis. Human herpesvirus type-8 (HHV-8) DNA was not detected in these cells. The patient achieved a complete remission with combination chemotherapy. Prior to the clinical onset of lymphoma, high fever of unknown origin had persisted for 21 months. IgG antibodies to EBV-viral capsid antigen and to EBV-early antigens, types D and R were not high (1:160 and less than 1:10, respectively). Two months after the onset of fever, however, retrospective quantitative PCR assay revealed a high EBV DNA load in plasma, indicating that CAEBV infection had been the cause of the patient's recurrent fever. The remarkable features of this case are (i) the development of lymphoma following CAEBV infection that demonstrated a normal pattern of EBV-specific antibodies, (ii) the development of HHV-8-negative body cavity lymphoma, and (iii) the effectiveness of combination chemotherapy.
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