HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Tovey, M. G. Articles by Gresser, I. Search for Related Content PubMed PubMed Citation Articles by Tovey, M. G. Articles by Gresser, I. Agricola Articles by Tovey, M. G. Articles by Gresser, I.

Interferon Enhances the Expression of Epstein—Barr Virus Early Antigen in Daudi Cells

Institut de Recherches Scientifiques sur le Cancer, Laboratory of Viral Oncology, BP8-94802 Villejuif, France

Treatment of the Burkitt lymphoma-derived cell line Daudi with highly purified human interferon- (IFN-) increased up to 100-fold the number of cells expressing Epstein—Barr virus (EBV)-determined early antigen (EA) without inducing the synthesis of virus capsid antigen (VCA), a late virus function. The increase in the number of EA-positive cells was proportional to interferon concentration up to 10⁴ international units (IU)/ml. Treatment of Daudi cells with the same number of units of either partially purified (sp. act. 10⁶ IU/mg protein) or electrophoretically pure (sp. act. 2 x 10⁸ IU/mg protein) IFN- both gave a similar increase in EA expression, strongly suggesting that the effects observed were indeed due to interferon. Furthermore, treatment of relatively interferon-insensitive Raji cells with IFN- (1 to 10⁴ IU/ml) had no significant effect on either spontaneous or 5-iodo-2'-deoxyuridine (IdUrd)-induced expression of EA or VCA. Human IFN- also enhanced the expression of EBV EA in Daudi cells. In contrast, when the latent EBV present in Daudi cells was activated to enter into a replicative cycle, either by induction with IdUrd or by superinfection with the non-transforming P₃HR1 strain of EBV, then treatment with human IFN- caused a marked inhibition of EA expression. Our results suggest that interferon can exert a differential action on virus replication depending upon the state of the virus genome within the cell.

Keywords: interferon, EBV, latency, virus induction

Received 21 October 1981; accepted 21 December 1981.