Transformation of foetal human leukocytes in vitro by filtrates of a human leukaemic cell line containing herpes‐like virus

Abstract

Transformation of foetal human leukocytes followed inoculation with a filtrate of cells of the QIMK-

Production of Human Monoclonal Antibody to X31 Influenza Virus Nucleoprotein

“…One method which has been used in attempts to produce human monoclonal antibodies is the infection of antibody-producing B lymphocytes with the Epstein-Barr (EB) virus. This virus is a human herpesvirus which only infects B lymphocytes (Pattengale et al, 1973), transforming them into lymphoblastoid cell lines with the capacity for indefinite growth in culture (Pope et al, 1968). These transformed cells synthesize and secrete immunoglobulin (Rosen et al, 1977), and recently this fact has been exploited to produce cell lines which secrete specific antibodies (Steinitz et al, 1977(Steinitz et al, , 1980Kozbor et al, 1979;Kozbor & Roder, 1981).…”

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

“…In vitro, EBV infects and transforms resting primary human B lymphocytes into continuously proliferating LCLs (Pope et al, 1968(Pope et al, , 1969reviewed in Rickinson and Kie , 1996). Recombinant EBV reverse genetic analyses in conjunction with in vitro B lymphocyte growth transformation assays have delineated the EBV genes necessary for transformation, while biochemical analyses have identi®ed cellular proteins that are involved in EBV-mediated transformation.…”

Non-correlation of in vivo and in vitro parameters of Epstein-Barr virus persistence suggests heterogeneity of B cell infection.

“…Epstein-Barr virus (EBV) is a lymphotropic herpesvirus which, on infection in vitro, immortalizes human B cells to yield continuously proliferating lymphoblastoid cell lines (LCL) (Pope et al, 1968). The majority of the human population undergo subclinical infection with EBV during childhood (Niederman et al, 1970), and the virus then establishes a lifelong persistent infection in two cellular sites -squamous epithelial cells and B lymphocytes (Sixbey, 1989).…”