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