EPSTEIN-BARR-VIRUS PERMISSIVELY INFECTS HUMAN SYNCYTIOTROPHOBLASTS IN-VITRO AND INDUCES REPLICATION OF HUMAN T-CELL LEUKEMIA-LYMPHOMA VIRUSTYPE-I IN DUALLY INFECTED-CELLS

Citation
Fd. Toth et al., EPSTEIN-BARR-VIRUS PERMISSIVELY INFECTS HUMAN SYNCYTIOTROPHOBLASTS IN-VITRO AND INDUCES REPLICATION OF HUMAN T-CELL LEUKEMIA-LYMPHOMA VIRUSTYPE-I IN DUALLY INFECTED-CELLS, Virology, 229(2), 1997, pp. 400-414
Citations number
74
Categorie Soggetti
Virology
Journal title
ISSN journal
00426822
Volume
229
Issue
2
Year of publication
1997
Pages
400 - 414
Database
ISI
SICI code
0042-6822(1997)229:2<400:EPIHSI>2.0.ZU;2-2
Abstract
Epstein-Barr virus (EBV) and human immunodeficiency virus type 1 (HIV- 1), as well as human T-cell leukemia-lymphoma virus type I (HTLV-I), m ay interact in the pathogenesis of human retroviral infections. The pl acental syncytiotrophoblast layer represents a barrier protecting the fetal compartment from exposure to retroviruses. We studied the intera ctions of EBV with HIV-I and HTLV-I in human term syncytiotrophoblast cells to investigate the significance of double infections in transpla cental transmission of human retroviruses. We found that syncytiotroph oblast cells could be productively infected with EBV. Dual infection o f the cells with EBV and HTLV-I resulted in full replication cycle of otherwise latent HTLV-I. In contrast, the restricted permissiveness of syncytiotrophoblasts for HIV-1 was not influenced by coinfection of t he cells with EBV. infection of syncytiotrophoblast cells with EBV, bu t not HTLV-I, induced interleukin-2 and interleukin-6 secretion, and a ugmented secretion occurred on coinfection with both viruses. Coinfect ion of syncytiotrophoblast cells with EBV and HTLV-I induced tumor nec rosis factor-beta and transforming growth factor-beta 1 secretion, but infection with either virus alone did not lead to secretion of these cytokines. Permissive replication cycle of HTLV-I was induced by the E BV immediate-early gene product Zta. Pseudotype formation between EBV and HTLV-I in coinfected syncytiotrophoblast cells was not found. Our data suggest: that activation of HTLV-I gene expression by EBV in coin fected syncytiotrophoblast cells may be a mechanism for transplacental transmission of HTLV-I. (C) 1997 Academic Press.