title: Reciprocal interactions between human cytomegalovirus and human T cell leukemia-lymphoma virus type I in monocyte-derived macrophages cultured in vitro.
abstract: Infection of macrophages with human cytomegalovirus (HCMV) has been shown to be nonlytic and exclusively cell associated. Human T cell leukemia-lymphoma virus type I (HTLV-I) is capable of establishing productive infection in macrophages. We studied the interactions between HCMV and HTLV-I in monocyte-derived macrophages cultured in vitro. We found that coinfection of macrophages with HCMV and HTLV-I significantly enhanced HCMV replication, resulting in release of infectious HCMV from dually infected cells. On the other hand, HCMV inhibited HTLV-I replication in macrophages coinfected with both viruses. Reciprocal interactions between HCMV and HTLV-I were mediated by their trans-acting proteins. Results of transfection studies demonstrated that the tax gene product of HTLV-I alone was capable of upregulating HCMV production. In a transient gene expression assay the immediate-early 2 (IE2) protein of HCMV alone could inhibit HTLV-I replication, whereas the IE1 protein, which had no effect by itself, produced a synergistic inhibitory effect together with the IE2 protein. Results from this study suggest that in vivo double infection of macrophages with HCMV and HTLV-I may contribute to the dissemination of HCMV infection in patients suffering from HTLV-I-associated T cell leukemia-lymphoma.
authors.affiliation: Institute of Microbiology, University Medical School, Debrecen, Hungary.
authors.forename: J
authors.initials: J
authors.lastname: Szabó
authors.forename: A
authors.initials: A
authors.lastname: Bácsi
authors.forename: I
authors.initials: I
authors.lastname: Andirkó
authors.forename: J
authors.initials: J
authors.lastname: Kiss
authors.forename: J
authors.initials: J
authors.lastname: Nemes
authors.forename: F D
authors.initials: FD
authors.lastname: Tóth
mesh_terms: D000956:Antigens, Viral / Q000378:metabolism; D002478:Cells, Cultured; D003587:Cytomegalovirus / Q000276:immunology / Q000502:physiology*; D015967:Gene Expression Regulation, Viral / Q000502:physiology; D016356:Gene Products, tax / Q000235:genetics / Q000378:metabolism; D015368:Human T-lymphotropic virus 1 / Q000276:immunology / Q000502:physiology*; D006801:Humans; D017874:Immediate-Early Proteins / Q000235:genetics / Q000378:metabolism; D008264:Macrophages / Q000821:virology*; D008562:Membrane Glycoproteins; D009000:Monocytes / Q000821:virology; D015534:Trans-Activators; D014162:Transfection; D014759:Viral Envelope Proteins; D014764:Viral Proteins; D014779:Virus Replication / Q000502:physiology*
chemical_list: D000956:Antigens, Viral; D016356:Gene Products, tax; C088645:IE1 protein, cytomegalovirus; C069186:IE2 protein, Cytomegalovirus; D017874:Immediate-Early Proteins; D008562:Membrane Glycoproteins; D015534:Trans-Activators; C077406:UL115 protein, Human herpesvirus 5; D014759:Viral Envelope Proteins; D014764:Viral Proteins; C071440:glycoprotein H, Cytomegalovirus; C499358:glycoprotein H, Human cytomegalovirus; C439068:glycoprotein O, cytomegalovirus