Open AccessPersistence of a Repressed Epstein-Barr Virus Genome in Burkitt Lymphoma Cells Made Resistant to 5-Bromodeoxyuridine
Author(s) -
Berge Hampar,
Jeffery G. Derge,
Lidia M. Martos,
John L. Walker
Publication year - 1971
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.68.12.3185
Subject(s) - thymidine kinase , epstein–barr virus , bromodeoxyuridine , biology , virus , virology , thymidine , microbiology and biotechnology , lymphoblast , antigen , dna , cell culture , genome , cell growth , genetics , gene , herpes simplex virus
The P3HR-1 line of human lymphoblastoid cells that is Epstein-Barr virus positive was made resistant to 5-bromodeoxyuridine. Epstein-Barr virus-associated antigens, but not virus particles, were produced in P3HR-1(BU) cells maintained on 5-bromodeoxyuridine. However, virus particles did appear within 4 days after removal of the drug. Thymidine kinase activity was limited to P3HR-1(BU) cells producing viral antigen, whereas all control P3HR-1 cells showed thymidine kinase activity regardless of viral antigen synthesis. Cellular DNA in most P3HR-1(BU) cells was made via pathways that did not involve thymidine kinase. In cells having a pathway that involved thymidine kinase, a second DNA of density 1.71 g/cm3 , corresponding to Epstein-Barr virus, was detected.It was concluded that: (a ) a repressed Epstein-Barr virus genome persists in P3HR-1(BU) cells that do not contain thymidine kinase, with activation of the viral genome being accompanied by productive infection and the appearance of enzyme, and (b ) thymidine kinase activity in P3HR-1(BU) cells could be used as a marker for viral genome expression.