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It takes decades after infection by HTLV-1 for an individual to develop adult T-cell
leukemia/lymphoma. This disease is associated with increase genomic instability, due
to an alteration of the DNA damage response of the infected cells. While this alteration
has been attributed to the viral protein Tax, we found that the viral protein HBZ
might also play a role in this process. In this study, we found that expression of
HBZ in Jurkat cells increases the sensitivity of these cells to Etoposide treatment.
Etoposide phosphate is an anticancer drug that induces DNA damage. This drug acts
by forming a ternary complex with DNA and Topoisomerase II, leading to inhibition
of the enzyme and creating double strand breaks. As a result, errors are incorporated
into the DNA and the cells undergo apoptosis. We treated a stable cell line expressing
HBZ, or the backbone vector, with 12.5μM Etoposide for 24 hrs. To determine the percentage
of viable cells as well as cells in early or late apoptosis, we used a combination
of Propidium iodide and Annexin V staining. Interestingly, we found that the cells
expressing HBZ exhibit a 16% increase in total apoptotic cells and a13 % increase
in late apoptotic cells compared to the cells expressing the backbone vector. This
result suggests that HBZ increases DNA damage following Etoposide treatment. Current
and future work investigates the effect of HBZ on other activators of the DNA damage
response and tries to delineate the effect of HBZ on the regulation of the DNA damage
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15th International Conference on Human Retroviruses: HTLV and Related Viruses