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Human lymphotropic viruses associated with lymphoid malignancy: Epstein-Barr and HTLV-1.
Hematol Oncol Clin North Am 1990; 4(4):821-33HO

Abstract

Epstein-Barr virus and HTLV-1 are both lymphotropic viruses, capable of immortalizing lymphocytes in vitro (Fig. 1). Both viruses have been sequenced and subjected to intense molecular biologic scrutiny, and in both cases genes believed to be important in lymphocyte immortalization have been identified. These viral genes are not homologues of cellular oncogenes, nor is there any evidence to suggest insertional mutagenesis. Rather, these genes alter the expression of a variety of cellular genes and, in so doing, alter the growth characteristics of the host cell. Infection with either virus is most likely to be asymptomatic, associated with a benign self-limited lymphoproliferation, or both, but in a small fraction of instances these benign lymphoproliferations give rise to a lymphoma or leukemia. In the case of the Epstein-Barr virus, a variety of cofactors have been identified that are important to the evolution of malignancy. These cofactors include immunosuppression in transplant recipients, cogenital immunodeficiency in the X-linked lymphoproliferative syndrome, human immunodeficiency virus infection in AIDS patients, and malaria in patients with endemic Burkitt's lymphoma. In the case of HTLV-1, cofactors have not been identified. Nonetheless, the importance of cofactors is suggested by the small fraction of the population infected by the virus who actually develop lymphoproliferative disease, and the long latency period between infection and the development of frank lymphoproliferative disease. In organ transplant recipients with lymphomas associated with Epstein-Barr virus infection, the EBV immortalizing/transforming genes are expressed in the malignant tissue. But in Burkitt's lymphoma and in adult T-cell leukemia/lymphoma, the EBV and HTLV-1 immortalizing/transforming genes are not detectably expressed. In Burkitt's lymphoma, it is suggested that the dysregulated myc gene renders the growth effects of Epstein-Barr virus latency genes superfluous. No comparable proto-oncogene translocation or activation has yet been identified in HTLV-1 lymphoma/leukemia.

Authors+Show Affiliations

Johns Hopkins University School of Medicine, Baltimore, Maryland.

Pub Type(s)

Comparative Study
Journal Article
Review

Language

eng

PubMed ID

2172203

Citation

Ambinder, R F.. "Human Lymphotropic Viruses Associated With Lymphoid Malignancy: Epstein-Barr and HTLV-1." Hematology/oncology Clinics of North America, vol. 4, no. 4, 1990, pp. 821-33.
Ambinder RF. Human lymphotropic viruses associated with lymphoid malignancy: Epstein-Barr and HTLV-1. Hematol Oncol Clin North Am. 1990;4(4):821-33.
Ambinder, R. F. (1990). Human lymphotropic viruses associated with lymphoid malignancy: Epstein-Barr and HTLV-1. Hematology/oncology Clinics of North America, 4(4), pp. 821-33.
Ambinder RF. Human Lymphotropic Viruses Associated With Lymphoid Malignancy: Epstein-Barr and HTLV-1. Hematol Oncol Clin North Am. 1990;4(4):821-33. PubMed PMID: 2172203.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Human lymphotropic viruses associated with lymphoid malignancy: Epstein-Barr and HTLV-1. A1 - Ambinder,R F, PY - 1990/8/1/pubmed PY - 1990/8/1/medline PY - 1990/8/1/entrez SP - 821 EP - 33 JF - Hematology/oncology clinics of North America JO - Hematol. Oncol. Clin. North Am. VL - 4 IS - 4 N2 - Epstein-Barr virus and HTLV-1 are both lymphotropic viruses, capable of immortalizing lymphocytes in vitro (Fig. 1). Both viruses have been sequenced and subjected to intense molecular biologic scrutiny, and in both cases genes believed to be important in lymphocyte immortalization have been identified. These viral genes are not homologues of cellular oncogenes, nor is there any evidence to suggest insertional mutagenesis. Rather, these genes alter the expression of a variety of cellular genes and, in so doing, alter the growth characteristics of the host cell. Infection with either virus is most likely to be asymptomatic, associated with a benign self-limited lymphoproliferation, or both, but in a small fraction of instances these benign lymphoproliferations give rise to a lymphoma or leukemia. In the case of the Epstein-Barr virus, a variety of cofactors have been identified that are important to the evolution of malignancy. These cofactors include immunosuppression in transplant recipients, cogenital immunodeficiency in the X-linked lymphoproliferative syndrome, human immunodeficiency virus infection in AIDS patients, and malaria in patients with endemic Burkitt's lymphoma. In the case of HTLV-1, cofactors have not been identified. Nonetheless, the importance of cofactors is suggested by the small fraction of the population infected by the virus who actually develop lymphoproliferative disease, and the long latency period between infection and the development of frank lymphoproliferative disease. In organ transplant recipients with lymphomas associated with Epstein-Barr virus infection, the EBV immortalizing/transforming genes are expressed in the malignant tissue. But in Burkitt's lymphoma and in adult T-cell leukemia/lymphoma, the EBV and HTLV-1 immortalizing/transforming genes are not detectably expressed. In Burkitt's lymphoma, it is suggested that the dysregulated myc gene renders the growth effects of Epstein-Barr virus latency genes superfluous. No comparable proto-oncogene translocation or activation has yet been identified in HTLV-1 lymphoma/leukemia. SN - 0889-8588 UR - https://www.unboundmedicine.com/medline/citation/2172203/Human_lymphotropic_viruses_associated_with_lymphoid_malignancy:_Epstein_Barr_and_HTLV_1_ DB - PRIME DP - Unbound Medicine ER -