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Erp57 facilitates ZIKV-induced DNA damage via NS2B/NS3 complex formation

Yiran Wang1, Dan Song1, Yichen Li1

  • 1Department of Biomedical Sciences, City University of Hong Kong, Hong Kong SAR, People's Republic of China.

Emerging Microbes & Infections
|October 15, 2024
PubMed

It is believed that DNA double-strand breaks induced by Zika virus (ZIKV) infection in pregnant women is a main reason of brain damage (e.g. microcephaly, severe brain malformation, and neuropathy) in newborn babies [1,2], but its underlying mechanism is poorly understood. In this study, we report that the depletion of ERp57, a member of the protein disulphide isomerase (PDI) family, leads to the limited production of ZIKV in nerve cells. ERp57 knockout not only suppresses viral induced reactive oxygen species (ROS) mediated host DNA damage, but also decreases apoptosis. Strikingly, DNA damage depends on ERp57-bridged complex formation of viral protein NS2B/NS3. LOC14, an ERp57 inhibitor, restricts ZIKV infection and virus-induced DNA damage. Our work reveals an important role of ERp57 in both ZIKV propagation and virus-induced DNA damage, suggesting a potential target against ZIKV infection.

Keywords:
DNA damageERp57ROSZIKA virusZIKV NS2B/NS3 complexantiviralapoptosis

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