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

Based on the phylogeny of viral sequences, ZIKV is classified into two major lineages, African and Asian [3] . First isolated in 1947 in Uganda [4] , ZIKVs of African lineage have rarely been associated with human cases, which typically exhibit an acute febrile illness. However, the outbreaks in the past decade of viruses of Asian lineage, not only greatly outnumbered the human infections known to be caused by the African virus but are notorious for their serious complications. Mounting evidence suggests that infection by ZIKV of Asian lineage is linked to congenital defects including microcephaly and spontaneous abortion [5] [6] [7] and to Guillain-Barre syndrome and thrombocytopenia in adults [8, 9] . Precisely how ZIKV causes these congenital and neurological disorders is unclear, but both viral and host factors have been suggested to play a role [10] . Of note, ZIKV replicates in neural progenitor cells, causing cell cycle arrest and/or death of neurons [10, 11] . Although mosquito bite is the most common route of ZIKV infection, ZIKV can also spread from person to person via sexual contact or vertically from pregnant woman to fetus [12] [13] [14] [15] . Consistent with these epidemiological findings, previous studies have revealed that ZIKV infects human skin cells, placental cells, endometrial stromal cells, etc. . . [11, [16] [17] [18] . Further studies on tissue tropism of the virus and factors regulating viral replication in and host responses of susceptible cell types are warranted, as they will yield novel insights into mechanisms of ZIKV pathogenesis and may identify therapeutic targets.