C19orf66 interrupts Zika virus replication by inducing lysosomal degradation of viral NS3.

ABSTRACT: The rapidly emerging human health crisis associated with the Zika virus (ZIKV) epidemic and its link to severe complications highlights the growing need to identify the mechanisms by which ZIKV accesses hosts. Interferon response protects host cells against viral infection, while the cellular factors that mediate this defense are the products of interferon-stimulated genes (ISGs). Although hundreds of ISGs have been identified, only a few have been characterized for their antiviral potential, target specificity and mechanisms of action. In this work, we focused our investigation on the possible antiviral effect of a novel ISG, C19orf66 in response to ZIKV infection and the associated mechanisms. We found that ZIKV infection could induce C19orf66 expression in ZIKV-permissive cells, and suc

SUBMITTER: Wu Y 

PROVIDER: S-EPMC7082052 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature