Plants are constantly exposed to pathogen attack and, in order to survive, have evolved complex defence mechanisms. Tomato yellow leaf curl virus (TYLCV) is a geminivirus with a small DNA genome (2.7 Kb) that forms minichromosomes and encodes six proteins, none of which is a DNA polymerase. Therefore, TYLCV relies on the plant cell machinery to replicate. The viral C3 protein acts as a replication enhancer through its interaction with the viral replication-associated protein, Rep, and with plant proteins. Interestingly, we found that C3 interacts with the Polycomb repressor complex (PRC) component LHP1 and with POLA2, a subunit of the DNA polymerase alpha, and interferes with the interaction between them; both LHP1 and POLA2 can bind the viral genome. H3K27me3, a repressive mark deposited by PRC, is decreased in both the plant and the viral genome upon TYLCV infection. PRC interacts with DNA replication-related proteins to maintain epigenetic repressive memory (H3K27me3) (Jian and Berger, 2017). Based on this model and our results, we hypothesize that plants may defend themselves against TYLCV via H3K27me3 deposition on the viral genome, and that C3 could inhibit this repression by uncoupling DNA replication from the action of the PRC complex. Since infection by geminiviruses also promotes replication of the plant genome, C3 may also relieve repressive memory to regulate the expression of host genes required for the viral infection.