Reciprocal interactions between human cytomegalovirus and human T cell leukemia-lymphoma virus type I in monocyte-derived macrophages cultured in vitro

• Published in: AIDS research and human retroviruses Vol. 14; no. 8; p. 699
• Main Authors: Szabó, J, Bácsi, A, Andirkó, I, Kiss, J, Nemes, J, Tóth, F D
• Format: Journal Article
• Language: English
• Published: United States 20.05.1998
• Subjects: Antigens, Viral - metabolism; Cells, Cultured; Cytomegalovirus - immunology; Cytomegalovirus - physiology; Gene Expression Regulation, Viral - physiology; Gene Products, tax - genetics; Gene Products, tax - metabolism; Human T-lymphotropic virus 1 - immunology; Human T-lymphotropic virus 1 - physiology; Humans; Immediate-Early Proteins - genetics; Immediate-Early Proteins - metabolism; Macrophages - virology; Membrane Glycoproteins; Monocytes - virology; Trans-Activators; Transfection; Viral Envelope Proteins; Viral Proteins; Virus Replication - physiology
• ISSN: 0889-2229
• DOI: 10.1089/aid.1998.14.699

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.