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. 1990 Jan;9(1):147-52.
doi: 10.1002/j.1460-2075.1990.tb08090.x.

An Epstein-Barr virus immortalization associated gene segment interferes specifically with the IFN-induced anti-proliferative response in human B-lymphoid cell lines

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An Epstein-Barr virus immortalization associated gene segment interferes specifically with the IFN-induced anti-proliferative response in human B-lymphoid cell lines

P Aman et al. EMBO J. 1990 Jan.

Abstract

Immortalization of human B-lymphocytes by Epstein-Barr virus (EBV) is associated with a decreased anti-proliferative response to interferon (IFN). In the present investigation we show that the resistance to the anti-proliferative effect of IFN class I on certain EBV-carrying Burkitt lymphoma cell lines is connected to the presence of the EBNA-2 gene and parts of the EBNA-5 gene of the EBV genome. Transfection of the genomic segment comprising these open reading frames into an IFN-sensitive lymphoma cell line demonstrated that it is sufficient to make cells resistant towards the antiproliferative effect of IFN class I. Expression of the EBNA-2 gene seems to be correlated with the IFN-resistant phenotype. The antiviral function of IFN, as tested by inhibition by vesicular stomatitis virus (VSV) infection, and the IFN-receptor binding are not suppressed. The present results suggest that the neutralization of the anti-proliferative effect of IFN-alpha is involved in the EBV-mediated immortalization of B-cells and that the anti-proliferative action of IFN class I does not necessarily recruit the same mechanism as the antiviral effect.

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References

    1. Int J Cancer. 1981 Nov 15;28(5):575-82 - PubMed
    1. J Gen Virol. 1975 Aug;28(2):207-17 - PubMed
    1. J Virol. 1988 Jan;62(1):114-9 - PubMed
    1. Int J Cancer. 1983 Jan 15;31(1):13-20 - PubMed
    1. J Virol. 1987 Dec;61(12):3870-8 - PubMed

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