Epstein-Barr virus-induced long-term proliferation of CD4-positive lymphocytes leading to T lymphoblastoid cell lines carrying latent Epstein-Barr virus (Meeting abstract).

Important note: Information in this article was accurate in 1998. The state of the art may have changed since the publication date.

Epstein-Barr virus-induced long-term proliferation of CD4-positive lymphocytes leading to T lymphoblastoid cell lines carrying latent Epstein-Barr virus (Meeting abstract).

Proc Annu Meet Am Assoc Cancer Res; 38:A1066 1997. Unique Identifier : AIDSLINE ICDB/98638066
Guan MX; Henderson EE; Department of Microbiology and Immunology, and the Fels Institute; for Cancer Research and Molecular Biology, Temple University; School of Medicine, Philadelphia, PA 19140

Abstract: The recent emergence of acquired immunodeficiency syndrome (AIDS)-related, Epstein-Barr virus (EBV)-associated T cell lymphomas as a new pathoclinical entity, conclusively demonstrates that EBV infection of T cells occurs in vivo. Whether the sequence of events leading to the emergence of EBV-carrying T cell lymphomas mirrors that for EBV-carrying B cell lymphomas remains to be determined. We have previously shown that CD4+ and CD8+ lymphocytes purified to near homogeneity from normal adult donors by flow cytometry could be infected with EBV. Infection with EBV was demonstrated by the accumulation of several components of the EBV replicative cycle, including viral DNA and viral transcripts encoding EBER1 and BRLF1. EBV infection occurred in primary T lymphocytes despite the lack of detectable CR2 or CR2 mRNA in T lymphocytes, suggesting the presence of a novel EBV receptor on T cells. Determining the mechanism whereby EBV contributes to these T cell lymphomas remains an elusive goal. Progress towards this goal would be advanced if a model for EBV-associated T cell proliferation could be developed. Here we describe EBV-induced long-term proliferation of CD4+ lymphocytes, leading to three established lymphoblastoid cell lines expressing T cell markers and carrying the EBV genome. In addition, mRNA encoding three EBV immediate-early transactivators could be detected using reverse transcription-polymerase chain reaction. Novel approaches to therapy of EBV-associated lymphomas based on EBV expression point out the importance of understanding EBV expression in T cells in developing therapy for these T cell lymphomas. Experiments were undertaken to determine whether EBV infection can alter the growth potential of T lymphocytes. Peripheral blood lymphocytes were separated into populations consisting of 99.8% CD4+ and 98.6% CD8+ T lymphocytes by FACS. Infection of these populations with EBV resulted in blastogenesis in both CD4+ and CD8+ populations in the presence of interleukin-2. Fifteen clones were established from the CD4+ population. Three of these clones expressed the T cell surface markers CD3, CD4 and carried the EBV genome. There was an absence of surface markers specific for B cells. In addition, the T cell lines transcribed mRNA encoding EBV immediate-early transactivators BYRF1, BMLF1, and BRLF1. These results demonstrate that EBV can both infect and induce growth transformation of T lymphocytes, supporting a direct role for EBV in Aids-related, EBV-associated T cell lymphomas. EBV can be added to the list of viruses, which includes herpes saimiri, which can induce human T cell proliferation in vitro.

Keywords: CD4-Positive T-Lymphocytes/*CYTOLOGY/VIROLOGY CD8-Positive T-Lymphocytes/*CYTOLOGY/VIROLOGY Cell Division DNA, Viral/ANALYSIS Genes, Immediate-Early Herpesviridae Infections/*GENETICS Herpesvirus 4, Human/*GENETICS Human Immediate-Early Proteins/GENETICS Lymphoma, T-Cell/*GENETICS/PATHOLOGY RNA-Binding Proteins/GENETICS Trans-Activators/GENETICS Transcription Factors/GENETICS Tumor Virus Infections/GENETICS ABSTRACT
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M9820762

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