The E3 ligase TRIM56 is a host restriction factor of Zika virus and depends on its RNA-binding activity but not miRNA regulation, for antiviral function

Yang, Darong; Li, Nan L.; Wei, Dahai; Liu, Baoming; Guo, Fang; Elbahesh, Husni; Zhang, Yunzhi; Zhou, Zhi; Chen, Guo-Yun; Li, Kui

The association of ZIKV infection with fetal microcephaly highlights the importance of neurotropism in ZIKV pathogenesis. In earlier work we found two human cell lines of neural origin, SK-N-SH and SVGA, to be permissive for ZIKV (S3 Fig). These offered tractable in vitro systems for evaluating the impact of TRIM56 on ZIKV infection in neural cells. SK-N-SH cells were transduced with control vector (Bsr) or Flag-TRIM56, followed by infection by ZIKV. Immunoblotting revealed viral E protein expression was substantially reduced in cells ectopically expressing Flag-TRIM56, as compared with control Bsr cells (Fig 8A, compare lanes 4 vs 3, and 6 vs 5). In agreement with this, progeny virus titers were significantly curtailed by TRIM56 overexpression (Fig 8B, compare bars 2 vs 1, and 4 vs 3, decreases of~6-8-fold) .