Activation of gene expression by human herpesvirus 6 is reporter gene-dependent.
Infection with human herpesvirus 6 (HHV-6) was found to up-regulate expression of human immunodeficiency 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.
Campbell
M E
ME
Department of Veterinary Pathology, Glasgow University, U.K.
McCorkindale
S
S
Everett
R D
RD
Onions
D E
DE
D015500:Chloramphenicol O-Acetyltransferase / Q000235:genetics; D002872:Chromosome Deletion; D004279:DNA, Viral / Q000235:genetics; D015967:Gene Expression Regulation, Viral; D005814:Genes, Viral; D015654:Herpesvirus 6, Human / Q000235:genetics* / Q000502:physiology; D015368:Human T-lymphotropic virus 1 / Q000235:genetics*; D009154:Mutation; D010957:Plasmids; D011401:Promoter Regions, Genetic; D014158:Transcription, Genetic; D014162:Transfection; D015854:Up-Regulation; D014779:Virus Replication
D004279:DNA, Viral; D015500:Chloramphenicol O-Acetyltransferase