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• Coxsackievirus B3 (CVB3) is a major pathogenic virus causing myocarditis, pancreatitis and meningitis. • Poly(rC) binding protein 1 (PCBP1) is a direct target of miR-21. • PCBP1 benefits CVB3 replication via blocking the translation of p62/SQSTM1. • Expression of PCBP1 is reduced by upregulated miR-21 upon CVB3 infection, which inhibits CVB3 replication. Coxsackievirus B3 (CVB3) is a positive single-strand RNA virus causing myocarditis, pancreatitis and meningitis. During CVB3 infection, various host cellular components, including proteins and non-coding RNAs, interact with the virus and affect viral infection. Poly(rC) binding protein 1 (PCBP1) is a multifunctional RNA binding protein regulating transcription, translation and mRNA stability of a variety of genes. In this study, we observed a significant reduction of PCBP1 protein during CVB3 infection. By bioinformatic prediction and luciferase-assay verification, we confirmed that the expression of PCBP1 was directly inhibited by miR-21, a microRNA upregulated during CVB3 infection. Furthermore, we found that overexpression of PCBP1 promoted CVB3 infection and knocking down of PCBP1 inhibited it. In the subsequent mechanism study, our results revealed that PCBP1 blocked the translation of p62/SQSTM1 (sequestosome 1), an autophagy-receptor protein suppressing CVB3 replication, by interacting with the cis-element in the 5′ untranslational region (5′ UTR) of p62/SQSTM1. In summary, our studies have identified PCBP1 as a beneficial factor for CVB3 infection. These findings may deepen the understanding of host-virus interactions and provide a potential target for intervention of CVB3 infection. [Display omitted] [ABSTRACT FROM AUTHOR]