There is no cure for diseases caused by retroviruses such as HIV-1, the infectious agent that has given rise to the human AIDS pandemic. Antiretroviral therapies can slow the progression of HIV/AIDS, but their usefulness is limited by their toxicity to human cells. The goal of our research is to identify highly specific targets for antiretroviral therapies by identifying replication mechanisms that are conserved among retroviruses and related endogenous retrotransposons but unnecessary for host cell replication or survival.