of Lymphoid Ma I i g n a ncies BACKGROUND. The Epstein-Barr virus (EBV) has been frequently detected in lymphoid malignancies. However, EBV infectioii in the nonneoplastic cells of lymphoid malignancies has not been extensively studied. ## METHODS. Four hundred nine cases of lymphoid malignancies
Replication of latent Epstein-Barr virus genomes in normal and malignant lymphoid cells
โ Scribed by Alice Adams; Tamara C. Pozos; Helen V. Purvey
- Publisher
- John Wiley and Sons
- Year
- 1989
- Tongue
- French
- Weight
- 617 KB
- Volume
- 44
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
โฆ Synopsis
DNA replication of 2 human lymphoid cell lines (U296 and Raji), latently infected with the Epstein-Barr virus, has been compared using a density transfer approach. Typical of nonmalignant lymphoblastoid cells, U296 cells divided once in bromodeoxyuridine-supplemented medium to form hybrid but not heavy-density host DNA. Replication of the intracellular Epstein-Barr virus DNA was selectively inhibited in these cells with only 15% of the viral genomes duplicating once to form hybrid-density viral DNA. However, some heavy-density viral DNA was formed in the U296 cells and DNA synthesis can thus initiate again on newly duplicated viral genomes in cells that have traversed only a single S phase. These re$ulb contrast strongly with observations concerning the Burkitt-lymphoma-derived cell line. Lymphoma cells are not growth-inhibited and most of the latent Epstein-Barr virus genornes of the Raji line replicated once, and only once, in succes$ive S phases. While the majority of the 50 Epstein-Barr virus genomes of both the Raji and U296 cell lines are maintained as extra-chromosomal DNA plasmids, the control of their duplication is distinctly different in the respective malignant and non-malignant host cells.
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