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Epstein-Barr virus (EBV)-induced long-term proliferation of CD4+ lymphocytes leading to T lymphoblastoid cell lines carrying EBV.
Anticancer Res. 1999 Jul-Aug; 19(4B):3007-17.AR

Abstract

We have previously demonstrated that Epstein-Barr virus (EBV) strain B95.8 can infect and initiate a partial transcriptional program in both CD4+ and CD8+ lymphocytes (Guan, M. X., R.-D. Zhang, B. Wu, and E. E. Henderson. 1996. J. Virol. 70:7341-7346). 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. Clones were established from the CD4+ population in the presence of interleukin-2. Two of these clones expressed the T cell surface markers CD3 and CD4 and carried the EBV genome. One lymphoblastoid cell line (LCL) had a mixture of CD4+ and CD19+ cells. The T-LCLs harboring the EBV genome in circular form and transcribed mRNA transcripts corresponding to BZLF1, BRLF1, BMLF1, and EBER-1 and -2. Immunofluorescence demonstrated EBNA in the nucleus of T rosette-positive lymphoblasts with an absence of viral capsid antigen expression. In situ hybridization for EBER showed nuclear and cytoplasmic staining in B95.8 cells, whereas EBV-carrying T-LCLs only showed nuclear staining. 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. A better understanding of the EBV transcriptional program during EBV-induced T cell transformation could directly lead to adoptive T cell therapeutic strategies and/or more effective antiviral chemotherapy for EBV-associated T cell lymphoma.

Authors+Show Affiliations

Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10652585

Citation

Guan, M, et al. "Epstein-Barr Virus (EBV)-induced Long-term Proliferation of CD4+ Lymphocytes Leading to T Lymphoblastoid Cell Lines Carrying EBV." Anticancer Research, vol. 19, no. 4B, 1999, pp. 3007-17.
Guan M, Romano G, Henderson EE. Epstein-Barr virus (EBV)-induced long-term proliferation of CD4+ lymphocytes leading to T lymphoblastoid cell lines carrying EBV. Anticancer Res. 1999;19(4B):3007-17.
Guan, M., Romano, G., & Henderson, E. E. (1999). Epstein-Barr virus (EBV)-induced long-term proliferation of CD4+ lymphocytes leading to T lymphoblastoid cell lines carrying EBV. Anticancer Research, 19(4B), 3007-17.
Guan M, Romano G, Henderson EE. Epstein-Barr Virus (EBV)-induced Long-term Proliferation of CD4+ Lymphocytes Leading to T Lymphoblastoid Cell Lines Carrying EBV. Anticancer Res. 1999 Jul-Aug;19(4B):3007-17. PubMed PMID: 10652585.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epstein-Barr virus (EBV)-induced long-term proliferation of CD4+ lymphocytes leading to T lymphoblastoid cell lines carrying EBV. AU - Guan,M, AU - Romano,G, AU - Henderson,E E, PY - 2000/2/1/pubmed PY - 2000/2/19/medline PY - 2000/2/1/entrez SP - 3007 EP - 17 JF - Anticancer research JO - Anticancer Res VL - 19 IS - 4B N2 - We have previously demonstrated that Epstein-Barr virus (EBV) strain B95.8 can infect and initiate a partial transcriptional program in both CD4+ and CD8+ lymphocytes (Guan, M. X., R.-D. Zhang, B. Wu, and E. E. Henderson. 1996. J. Virol. 70:7341-7346). 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. Clones were established from the CD4+ population in the presence of interleukin-2. Two of these clones expressed the T cell surface markers CD3 and CD4 and carried the EBV genome. One lymphoblastoid cell line (LCL) had a mixture of CD4+ and CD19+ cells. The T-LCLs harboring the EBV genome in circular form and transcribed mRNA transcripts corresponding to BZLF1, BRLF1, BMLF1, and EBER-1 and -2. Immunofluorescence demonstrated EBNA in the nucleus of T rosette-positive lymphoblasts with an absence of viral capsid antigen expression. In situ hybridization for EBER showed nuclear and cytoplasmic staining in B95.8 cells, whereas EBV-carrying T-LCLs only showed nuclear staining. 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. A better understanding of the EBV transcriptional program during EBV-induced T cell transformation could directly lead to adoptive T cell therapeutic strategies and/or more effective antiviral chemotherapy for EBV-associated T cell lymphoma. SN - 0250-7005 UR - https://www.unboundmedicine.com/medline/citation/10652585/Epstein_Barr_virus__EBV__induced_long_term_proliferation_of_CD4+_lymphocytes_leading_to_T_lymphoblastoid_cell_lines_carrying_EBV_ L2 - https://antibodies.cancer.gov/detail/CPTC-CD4-1 DB - PRIME DP - Unbound Medicine ER -