Novel coronavirus (SARS-CoV-2) infection increases the risk of myocardial injury, and the mole-cular mechanisms of pathogenesis remain to be elucidated. Herein, the changes of RNA editing in SARS-CoV-2 infected cardiomyocytes (infection group) and uninfected cardiomyocytes (mock group) were compa-red to explore the effects of the viral infection on cardiomyocytes from the perspective of RNA editing. RNA-seq data (GSE150392) of SARS-CoV-2 infection of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) was downloaded from the GEO database, and RNA editing sites (RESs) were iden-tified using SPRINT software. The changes in editing levels of cardiomyocytes in the infection and mock groups were compared, editing sites were annotated, and relevant functional analyses were performed. A total of about 92 899 base substitutions were detected, of which 87 670 were identified as A-to-I RESs, and 78 978 of these A-to-I editing sites were found to appear in the Alu regions. A-to-I editing sites tend to be dis-tributed in clusters, mainly in regions such as introns and intergenic regions. By screening the differential RESs between the infection and mock groups in A-to-I editing, it was found that 102 of the significantly differential RESs are up-regulated and 94 are down-regulated in editing level. These genes with significant differences in RES are involved in the biological processes of viral infection related GO (Gene Ontology), which are mainly enriched in viral process, virus life cycle, and defense response to virus, et al., and their Kyoto Encyclopedia of Genes and Genomes (KEGG) functional pathways are also mainly related to viral infec-tion. In contrast, the 11 screened genes with high-quality A-to-I RESs and significant differences in editing levels between groups are enriched in endocytosis, cytokine-cytokine receptor interaction, proteosome, nico-tinate and nicotinamide metabolism, and ferroptosis, et al.. The results showed that SARS-CoV-2 infection affects A-to-I RNA editing in cardiac myocytes, and the occurrence of such RNA editing events is a re-sponse of host cardiac myocytes to the viral infection.