Taken into account the neurotropism of ZIKV infection in vivo, our revelations that TRIM56 was basally expressed in human brain [25], human astrocytes SVGA and primary mouse neurons (this study) and that its expression was elevated following ZIKV infection in neural cell types support the biological relevance of TRIM56 as a host restriction factor of ZIKV. Here, TRIM56 is linked to Zika virus infectious disease.