ABSTRACT. Infertility is a problem that affects one out of five couples, yet the cause of sterility is unknown in 30% of cases. One threat to viable gamete development is activity of a subset of transposons known as endogenous retroviruses (ERVs). ERVs have the ability to self-replicate and sometimes mobilize, creating new genomic insertions within the same cell or even neighboring cells. Previous studies have demonstrated that, in Drosophila, ERV activation within the follicle cells of developing eggs causes sterility. The current explanation for ERV-triggered sterility postulates that ERVs migrate from the follicle cells into the oocyte and insert themselves into new genomic loci, damaging DNA integrity. However, our lab has found no evidence of novel ERV insertions being made into the oocyte genome, suggesting sterility may arise from uncharacterized mechanism(s). Here, we propose an alternative explanation for transposon-triggered sterility: we hypothesize that ERV derepression induces sterility through activation of an aberrant immune response. We found that depletion of key immune pathway components rescued fertility despite ERV hyperactivity. These data provide evidence that transposon-triggered sterility may be due to immune activation rather than DNA damage within the oocyte. This proposal seeks to investigate how the immune system recognizes ERVs and whether that immune response can cause sterility. Ultimately, these findings may provide an alternative explanation for ERV-triggered sterility as well as advance our understanding of how ERVs impact human health.