Bidirectional enhancing activities between human T cell leukemia-lymphoma virus type I and human cytomegalovirus in human term syncytiotrophoblast cells cultured in vitro. NLM AIDSLINE Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.

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Bidirectional enhancing activities between human T cell leukemia-lymphoma virus type I and human cytomegalovirus in human term syncytiotrophoblast cells cultured in vitro.

AIDS Res Hum Retroviruses. 1995 Dec;11(12):1495-1507. Unique Identifier : AIDSLINE MED/96288449
Toth FD; Aboagye-Mathiesen G; Szabo J; Liu X; Mosborg-Petersen P; Kiss J; Hager H; Zdravkovic M; Andirko I; Aranyosi J; et al; Department of Virus and Cancer, Danish Cancer Society, Aarhus,; Denmark.


Abstract: The syncytiotrophoblast layer of the human placenta has an important role in limiting transplacental viral spread from mother to fetus. Human cytomegalovirus (HCMV) is capable of establishing a latent infection in syncytiotrophoblast cells, with restriction of gene expression to immediate-early and early proteins. We analyzed the extent of replication of human T cell leukemia-lymphoma virus type I (HTLV-I) in human term syncytiotrophoblasts infected with HTLV-I alone or coinfected with HTLV-I and HCMV. Although syncytiotrophoblasts could be infected with cell-free HTLV-I, no viral protein expression was found in the singly infected cells. On the contrary, coinfection of the cells with HTLV-I and HCMV resulted in simultaneous replication of both viruses. Bidirectional enhancing activities between HTLV-I and HCMV were mediated primarily by the Tax and immediate-early proteins, respectively. The stimulatory effect of HTLV-I Tax on HCMV replication appeared to be mediated partly by tumor necrosis factor beta and transforming growth factor beta-1. We observed formation of pseudotypes with HTLV-I nucleocapsids within HCMV envelopes, whereas HCMV was not pseudotyped by HTLV-I envelopes in dually infected syncytiotrophoblast cells. Our data suggest that in vivo dual infection of syncytiotrophoblast cells with HTLV-I and HCMV may facilitate the transplacental transmission of both viruses.
Keywords: Antibodies, Monoclonal/PHARMACOLOGY Base Sequence Cells, Cultured Cytokines/BIOSYNTHESIS Cytomegalovirus/*GROWTH & DEVELOPMENT/PATHOGENICITY Gene Products, tax/PHYSIOLOGY Human HTLV-I/*GROWTH & DEVELOPMENT/PATHOGENICITY Immediate-Early Proteins/IMMUNOLOGY/PHYSIOLOGY Immune Sera Interleukin-2/IMMUNOLOGY/PHYSIOLOGY Lymphotoxin/IMMUNOLOGY/PHYSIOLOGY Molecular Sequence Data Placenta/*VIROLOGY Polymerase Chain Reaction Support, Non-U.S. Gov't Transforming Growth Factor beta/IMMUNOLOGY/PHYSIOLOGY Virus Latency Virus Replication JOURNAL ARTICLEKWDantibodies,monoclonal/pharmacologybasesequencecells,culturedcytokines/biosynthesiscytomegalovirus/KWDgrowth&development/pathogenicitygeneproducts,tax/physiologyhumanhtlv-i/KWDgrowth&development/pathogenicityimmediate-earlyproteins/immunology/physiologyimmuneserainterleukin-2/immunology/physiologylymphotoxin/immunology/physiologymolecularsequencedataplacenta/KWDvirologypolymerasechainreactionsupport,non-uKWDsKWDgov'ttransforminggrowthfactorbeta/immunology/physiologyviruslatencyvirusreplicationjournalarticle
961030
M96A0721

Copyright © 1996 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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