Type 1 Diabetes (T1D) is characterised by the destruction of insulin-producing islet beta cells. Islet autoimmunity (IA) is defined by the presence of autoantibodies occurring prior to T1D, although progression from IA to T1D is dynamic and individuals can remain asymptomatic. Environmental factors, including viral infections, have been theorised to be contributing to IA and T1D, as genetics alone cannot fully explain the development of the disease. This study investigates the relationship between the history of viral infections and IA onset in children using VirScan, an application of phage immunoprecipitation sequencing (PhIP-Seq), and AntiViral Antibody Response Deconvolution Algorithm (AVARDA) to correctly identify viral species targeted by plasma antibodies. Participants were selected from the Australian Viruses In the Genetically at Risk (VIGR) birth cohort, including 21 individuals with IA and matched controls. Antibody peptides against 93 virus species were identified, but no significant differences were found in targeted viral species between cases and controls. However, cases exhibited unique viral epitopes, particularly for enteroviruses and rhinoviruses, suggesting a differential immune response against the same viruses, also supported by the small number of shared epitopes (~45%). Differential expression analysis of peptides aligning to a reference enterovirus genome also show protein regions of this virus have an increased response in cases compared to controls. In addition, after IA seroconversion, multiple unique peptide targets against enteroviruses were detected in cases compared to a previous time point and their matching controls. This study suggests that the immune response to viral infections may play a role in the onset of IA and highlights the need for further research to understand the mechanisms of viral-induced autoimmunity in T1D.