title: Bidirectional enhancing activities between human T cell leukemia-lymphoma virus type I and human cytomegalovirus in human term syncytiotrophoblast cells cultured in vitro.
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.
authors.affiliation: Department of Virus and Cancer, Danish Cancer Society, Aarhus, Denmark.
authors.forename: F D
authors.initials: FD
authors.lastname: Tóth
authors.forename: G
authors.initials: G
authors.lastname: Aboagye-Mathiesen
authors.forename: J
authors.initials: J
authors.lastname: Szabó
authors.forename: X
authors.initials: X
authors.lastname: Liu
authors.forename: P
authors.initials: P
authors.lastname: Mosborg-Petersen
authors.forename: J
authors.initials: J
authors.lastname: Kiss
authors.forename: H
authors.initials: H
authors.lastname: Hager
authors.forename: M
authors.initials: M
authors.lastname: Zdravkovic
authors.forename: I
authors.initials: I
authors.lastname: Andirkó
authors.forename: J
authors.initials: J
authors.lastname: Aranyosi
mesh_terms: D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001483:Base Sequence; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis; D003587:Cytomegalovirus / Q000254:growth & development* / Q000472:pathogenicity; D016356:Gene Products, tax / Q000502:physiology; D015368:Human T-lymphotropic virus 1 / Q000254:growth & development* / Q000472:pathogenicity; D006801:Humans; D017874:Immediate-Early Proteins / Q000276:immunology / Q000502:physiology; D007106:Immune Sera; D007376:Interleukin-2 / Q000276:immunology / Q000502:physiology; D008233:Lymphotoxin-alpha / Q000276:immunology / Q000502:physiology; D008969:Molecular Sequence Data; D010920:Placenta / Q000821:virology*; D016133:Polymerase Chain Reaction; D016212:Transforming Growth Factor beta / Q000276:immunology / Q000502:physiology; D017735:Virus Latency; D014779:Virus Replication
chemical_list: D000911:Antibodies, Monoclonal; D016207:Cytokines; D016356:Gene Products, tax; D017874:Immediate-Early Proteins; D007106:Immune Sera; D007376:Interleukin-2; D008233:Lymphotoxin-alpha; D016212:Transforming Growth Factor beta