@article{mbs:/content/journal/jgv/10.1099/0022-1317-74-4-715, author = "Feng, Chu-Pei and Kulka, M. ichael. and Aurelian, L. aure.", title = "The GGTCA palindrome and cognate cellular factors in trans-regulation of human immunodeficiency virus long terminal repeat by herpes simplex virus", journal= "Journal of General Virology", year = "1993", volume = "74", number = "4", pages = "715-723", doi = "https://doi.org/10.1099/0022-1317-74-4-715", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-74-4-715", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "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.", }