Activation of gene expression by human herpesvirus 6 is reporter gene-dependent
Campbell, Moyra E. M. and McCorkindale, Stewart and Everett, Roger D. and Onions, David E.,, 72, 1123-1130 (1991),
doi = https://doi.org/10.1099/0022-1317-72-5-1123,
publicationName = Microbiology Society,
issn = 0022-1317,
abstract= Infection with human herpesvirus 6 (HHV-6) was found to up-regulate expression of human immuno-deficiency virus and human T cell leukaemia virus type I (HTLV-I) long terminal repeat sequence (LTR), and herpes simplex virus type 1 (HSV-1) gD chloramphenicol acetyltransferase (CAT) constructs transfected into the T cell line, J. Jhan. Activation by HHV-6 was due to one or more viral proteins produced early in infection and, in the case of the HTLV-I LTR, was synergistic to induction mediated by the HTLV-I tax gene product. Neither the HTLV-I enhancer nor basal promoter elements of the HSV-1 gD gene were essential for activation and no increase in accumulated HTLV-I mRNA was observed due to HHV-6 infection. Induction by HHV-6 was found to be dependent on the reporter construct used, because the CAT gene and, to a lesser extent, the HSV-1 thymidine kinase gene were responsive to HHV-6 infection although no significant activation of growth hormone constructs was observed. Our results bear a strong resemblance to those obtained for the Epstein-Barr virus BMLF1 gene, indicating that the major HHV-6 trans-activator may be a homologue of this gene.,
language=,
type=