During CVB infection, previous data showed that AUF1 was not only recruited into stress granules (SGs) [10] that formed in host cells under unfavorable stimulation, such as virus infection [11], and affected mRNA localization, translation and degradation, as well as signaling pathways and antiviral responses [12]; AUF1 was also reported to negatively regulate viral infection by inhibiting viral translation [3]. This evidence concerns the gene HNRNPD and viral infectious disease.