Cancer is derived from a single cell that carries mutations that drive an uncontrolled increase in cell number. Recent research has revealed that a surprisingly high number of mutations also accumulate in healthy tissues as we age. For example, by the age of 50, the genetic material of the average white blood cell has accumulated between 800-1,600 mutations. It is thought that mutations that cause cancer have a more profound impact on cell behaviour than mutations found in healthy tissue; however, research is ongoing, and many open questions remain. Viruses cause around 10% of cancers. Therefore, it is vital to investigate how viral infection impacts the burden of mutations in healthy tissue and virus-related cancer. This has been technically challenging to do in humans, as it requires obtaining samples at different stages of infection and cancer development. In this project, I will investigate the consequences of persistent infection with of a cancer-causing virus, Human T cell leukaemia virus type-1 (HTLV-1), on the genetic material of human blood cells. Because HTLV-1 infects cells that circulate in the blood, they can be easily collected and grown in the lab, enabling us to map the locations where mutations occur in each cell's genes. We will study cells from healthy carriers of the virus and cells from people who are in the process of developing Adult T cell Leukaemia/Lymphoma. This analysis will reveal whether the virus changes the type of mutations and the rate at which mutations occur within infected cells, identify if certain mutations are associated with changes in cell behaviour, and can indicate which cellular processes caused the mutations. This research will allow us for the first time to gain direct insight into how HTLV-1 disrupts the genetic material of otherwise healthy cells which it infects, and is key to understanding how HTLV-1 and other similar viruses cause cancer.