BCL-2 induction is part of the strategy of Epstein-Barr virus.
Epstein Barr virus can infect B lymphocytes and epithelial cells. Epithelial cells present the natural reservoir for the virus in man. In vitro, infected cells harbor the virus predominantly in a latent state with the expression of a set of nuclear (EBNA 1-6) and latent membrane genes (LMP 1-2) and virus-transformed B cells grow as permanently immortalized lymphoblastoid cell lines, that show increased resistance to various growth inhibiting factors. Here we show that the lymphoma-associated oncogene BCL-2 is upregulated by different latent Epstein-Barr virus genes in B lymphocytes as well as keratinocyte cell lines. Thus, the induction of BCL-2 gene expression seems to be part of the survival strategy of the virus independently of the host cell infected.
Finke
J
J
Department of Hematology and Oncology, University of Freiburg, Germany.
Lange
W
W
Mertelsmann
R
R
Dölken
G
G
D001402:B-Lymphocytes / Q000378:metabolism; D001483:Base Sequence; D002460:Cell Line; D004854:Herpesvirus 4, Human / Q000235:genetics*; D006801:Humans; D015603:Keratinocytes / Q000378:metabolism; D008969:Molecular Sequence Data; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D019253:Proto-Oncogene Proteins c-bcl-2; D011519:Proto-Oncogenes; D014162:Transfection
D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2