Lymphoproliferative disorders in heart transplant recipients: role of hepatitis C virus (HCV) and Epstein-Barr virus (EBV) infection

2000 ◽  
Vol 13 (0) ◽  
pp. S402-S405 ◽  
Author(s):  
A. Buda ◽  
A. Caforio ◽  
F. Calabrese ◽  
S. Fagiuoli ◽  
S. Pevere ◽  
...  
1993 ◽  
Vol 4 (suppl c) ◽  
pp. 33-40
Author(s):  
F Diaz-Mitoma

Immunosuppressed patients are at risk of severe herpesvirus infections. Herpes simplex (HSV), varicellazoster (VZV) and Epstein-Barr virus (EBV) infections are associated with characteristic syndromes in this population. Typically I-ISV and VZ:V infections cause mucocutaneous lesions; diagnosis is usually con finned by tissue culture or nuorescent microscopy. The availability of effective antiviral agents, and accurate techniques for laboratory diagnosis have improved the management of I-ISV and VZ:V infections. Antibody assays to demonstrate I-ISVorVZ:V infections are of limited value in immunocompromised patients, because the presence of antibodies does not indicate a decreased risk for HSV, varicella or zoster, but indicates susceptibility for reactivated infection. EBV is associated with lymphoproliferative disorders in transplant recipients. Infection of lymphocytes by EBV is a necessary step in achieving B cell transformation and immortalization. The lack of immunosurveillance against EBV-transformed B cells predisposes patients to developing invasive infiltration of transformed B cells . Diagnostic methods for EBV infections include lymphocyte transfom1ation, serology, and detection of DNA by direct hybridization or by DNA amplification. Quantitative oropharyngeal EBV shedding is a good marker for the development of lymphoproliferative disease in transplant recipients. Patients experiencing primary EBV infection are at the highest risk for lymphoproliferative disorders. Prophylactic antiviral therapy may be of benefit in preventing EBV replication and therefore in decreasing the risk for lymphoproliferation.


Blood ◽  
1993 ◽  
Vol 81 (5) ◽  
pp. 1393-1403 ◽  
Author(s):  
H Cen ◽  
PA Williams ◽  
HP McWilliams ◽  
MC Breinig ◽  
M Ho ◽  
...  

Epstein-Barr virus (EBV) is associated with the development of two human B-cell malignancies, Burkitt's lymphoma and lymphomas that occur in the immunosuppressed host. The latter category of disease has become important recently as it is seen primarily in organ transplant recipients and individuals with acquired immunodeficiency syndrome. One possible mechanism for lymphoma development involves a reduction in or lack of EBV-specific cytotoxic T-cell recognition. In support of this model are previous observations that the expression of EBV nuclear antigen 2 (EBNA2) and latent membrane protein, two viral antigens associated with major histocompatibility complex class I-restricted T- cell killing, are downregulated in Burkitt's lymphoma and in early passage lymphoblastoid cell lines (LCL) derived from the malignant lesions. To determine whether a similar mechanism could occur in the development of posttransplant lymphoproliferative disorders (PTLD), we compared EBV gene expression among 23 PTLD tumor lesions obtained from 11 solid organ transplant recipients and among LCL derived from 3 of these lesions. In this report, we demonstrate, by Southern blot, Western blot, and immunofluorescence analysis, that (1) the tumor lesions exhibit varying patterns of restricted viral gene expression; (2) LCL derived from these lesions may represent the in vitro selection of cell subpopulations; and (3) immunosuppressed individuals have a markedly reduced antibody response to the latent cycle antigens, EBNA1, EBNA2, and EBNA-LP, but not to the lytic cycle viral capsid antigen when compared with normal immunocompetent controls.


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