The GGTCA palindrome and cognate cellular factors in trans-regulation of human immunodeficiency virus long terminal repeat by herpes simplex virus

• Published in: Journal of general virology 1993-04, Vol.74 (4), p.715-723
• Main Authors: Feng, Chu-Pei, Kulka, Michael, Aurelian, Laure
• Format: Article
• Language: English
• Subjects: AIDS/HIV; Base Sequence; Biological and medical sciences; DNA-Binding Proteins - metabolism; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation, Viral; HIV Long Terminal Repeat - genetics; HIV-1 - genetics; Humans; In Vitro Techniques; Microbiology; Molecular Sequence Data; Monocytes - microbiology; Nuclear Proteins - metabolism; Oligodeoxyribonucleotides - chemistry; Regulatory Sequences, Nucleic Acid; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains; RNA, Messenger - genetics; Simplexvirus - genetics; Tumor Cells, Cultured; Virology
• ISSN: 0022-1317; 1465-2099
• DOI: 10.1099/0022-1317-74-4-715

1 Virology/Immunology Laboratories, Department of Pharmacology and Experimental Therapeutics and 2 Department of Microbiology and Immunology, The University of Maryland, School of Medicine, Baltimore, Maryland 21201, U.S.A. Molecular interactions between herpes simplex virus type 1 (HSV-1) and human immunodeficiency virus (HIV) were investigated in the promonocytic cell line U937. HSV-1-mediated activation was observed in transient expression assays with hybrid constructions containing the HIV long terminal repeat (LTR)-directed chloramphenicol acetyltransferase gene. Comparison of constructions that differ in the GGTCA palindrome located within the negative regulatory region of the LTR revealed four- to eightfold lower activation levels for the wild-type as compared to the mutant sequence. Three protein species, 37K, 59K/64K and 75K, that bind to the wild-type GGTCA palindrome were resolved in nuclear extracts of uninfected U937 cells by gel retardation and u.v.-crosslinking experiments. The 37K protein did not bind to the mutant palindrome sequence. However, a distinct 120K protein was detected. The 37K and 59K/64K binding proteins were not resolved in similar experiments performed with nuclear extracts from HSV-1-infected U937 cells but there was a novel p50 species that binds only to the wild-type palindrome sequence. These findings raise the possibility that interaction of these proteins at the GGTCA palindrome is involved in HSV-1-mediated regulation of the HIV LTR in U937 cells. Received 28 April 1992; accepted 10 November 1992.