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Human T-cell leukemia virus type 1 (HTLV-1) basic leucine zipper factor (HBZ) is transcribed
from the antisense genomic DNA strand and functions differently in its RNA and protein
forms. To distinguish between the roles of hbz mRNA and HBZ protein, we generated
mutants in a proviral clone that specifically disrupt the hbz gene product. A proviral
clone with a splice acceptor mutation that disrupts expression of the predominant
hbz mRNA resulted in lower levels of tax mRNA. Heterologous hbz expression restored
Tax activity in cells expressing this mutant clone. In contrast, proviral mutants
that disrupt only HBZ protein did not affect levels of tax mRNA. Expression of hbz
resulted in lower levels of p30II mRNA. Mutation of p30II overcame the effects of
the splice acceptor mutation of hbz, and restored tax expression. Thus, there is a
complex interplay of viral regulatory proteins controlling levels of HTLV-1 gene expression.
The pathogenic role of HBZ alone or combined with Tax is currently under study in
transgenic mice, and will be discussed.
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15th International Conference on Human Retroviruses: HTLV and Related Viruses