Herpes-Type Virus and Chromosome Marker in Normal Leukocytes after Growth with Irradiated Burkitt Cells

Abstract

Cultured cells derived from male patients with Burkitt's lymphoma and harboring herpes-type virus particles were lethally irradiated. These irradiated cells induced normal peripheral leukocytes of female infants to grow within 2 to 4 weeks after mixed cultivation. Cells of a line free of this agent failed to stimulate growth. If either type of cell was cultured separately, it did not survive under the experimental conditions. Herpes-type viral antigen and C-group chromosomal marker previously described in cultured Burkitt cells were found in all of the female cell cultures that were obtained.

Further evidence of space-time clustering of Burkitt's lymphoma patients in the West Nile District of Uganda.

“…Possibly the most important finding is that when normal leukocytes are cultured with Epstein-Barr virus (EBV)-first discovered in Burkitt's tumour cell lines-cells descended from them mimic the behaviour of malignant cells in vitro (Henle et al, 1967). This makes EBV a strong candidate for a crucial causative role in Burkitt's lymphoma.…”

Epstein-Barr virus transformation: involvement of latent membrane protein 1-mediated activation of NF-κB

“…Although the primary infection is controlled principally by an antiviral T-cell response, EBV persists for the lifetime of the individual by infecting and establishing a latent infection in memory B lymphocytes (Babcock et al, 1998;Nilsson et al, 1971;Rickinson et al, 1975Rickinson et al, , 1980Yao et al, 1989). B lymphocytes latently infected with EBV have the potential to produce inde®nitely proliferating lymphocytes as evidenced by the outgrowth of EBV-transformed lymphoblastoid cell lines (LCLs) when peripheral blood B lymphocytes are cultured in vitro (Henle et al, 1967). For most people, latent infection is innocuous due to constant immune surveillance of infected cells.…”

Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16 INK4A and p14 ARF expression

“…1). In primary human infection, and in vitro, EBV latency III infection converts B cells into proliferating lymphoblast cell lines (LCLs) (2,3). In LCLs, EBV expresses six nuclear antigen proteins (EBNA2, EBNALP, EBNA3A, EBNA3B, EBNA3C, and EBNA1), two latent infection membrane proteins (LMP1 and LMP2), two small RNAs (EBER1 and EBER2), and BamHI A rightward transcripts (BARTs).…”