Sensitivity to ebv superinfection and IUdR inducibility of hybrid cells formed between a sensitive and a relatively resistant burkitt lymphoma cell line

✍ Scribed by Okot Nyormoi; George Klein; Alice Adams; Laszlo Dombos

• Publisher: John Wiley and Sons
• Year: 1973
• Tongue: French
• Weight: 1020 KB
• Volume: 12
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910120211

✦ Synopsis

Abstract

The sensitivity of Burkitt lymphoma‐derived cell lines to Epstein‐Barr virus (EBV) superinfection and the inducibility of the latent EBV genome in these lines were studied by somatic cell hybridization. Two non‐EBV producer lines; AG R3, an adherent, 8‐azaguanine‐resistant variant of the Rajiline; and Namalwa, a non‐adherent, 8‐azaguanine‐sensitive line, were fused with the aid of β‐propiolactone‐inactivated Sendai virus. The resident EBV genome in Raji is inducible with 5‐iododeoxyuridine and the line is also sensitive to EBV superinfection. Namalwa is relatively resistant to both super‐infection and induction, and synthetizes surface‐associated IgM‐lambda. Cytological studies showed that hybrid cells appear to be much larger than either parent and attach to culture plates less firmly than the adherent Raji variant parent. Karyological analyses showed that hybrids contain the expected sum of the parental chromosome markers. Membrane immunofluorescence tests also showed that hybrids synthetize IgM. All the hybrid cells appear to be non‐EBV producers, but they are sensitive to both EBV super‐infection and induction of latent EBV. These findings suggest the following explanations: (1) there is no evidence of any complementation between the two non‐EBV producer lines (Raji and Namalwa) to elicit spontaneous EBV production in hybrid cells; (2) Namalwa is deficient in some factors required for the synthesis of EBV‐specified early antigens after EBV superinfection and after induction of latent EBV by IUdR; these factors are supplied by the Raji parent in the hybrids; or (3) Raji, Namalwa and hybrid cells or EBV all produce a substance which inhibits activation of a productive viral cycle, but whose action is antagonized in Raji and hybrid cells to allow the synthesis of EBV‐specific early antigens.