Viruses, as obligate intracellular parasites, rely on a host cell for their replication. Viruses must manipulate the host cell by hijacking, inhibiting, or repurposing its molecular machinery, thereby creating an environment conducive to viral multiplication. Among other tasks, viruses need to effectively suppress plant anti-viral mechanisms, which include chloroplast-mediated defences. We have found that the plant DNA geminivirus tomato yellow leaf curl virus (TYLCV) encodes a protein, C4, which re-localizes from the plasma membrane to chloroplasts upon activation of defence. In chloroplasts, C4 interacts with the plant calcium sensing receptor (CAS) and suppresses retrograde signaling and the downstream activation of salicylic acid (SA)-dependent defence, promoting viral infection (Medina-Puche et al., 2020). Multiple other geminiviruses encode C4 homologues that localize in chloroplasts and affect this organelle in different manners: for example, while the C4 proteins from East African cassava mosaic virus and beet curly top virus behave like that of TYLCV, translocating to chloroplasts and interfering with retrograde signalling (Medina-Puche et al., 2020), the positional homologue from tomato golden mosaic virus hijacks the ubiquitination machinery to induce chloroplast degradation (Mei et al., 2024), and that from African cassava mosaic virus induces conspicuous accumulation of starch. Following comparison of the C4 proteins from nine different geminivirus species, our results suggest that chloroplasts are a prevalent target of geminiviruses, which have evolved different strategies to interfere with chloroplast-dependent defences.