Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Zika Virus Induces the Degradation of the Numb Protein that is Required through Embryonic Neurogenesis

Version 1 : Received: 14 April 2023 / Approved: 17 April 2023 / Online: 17 April 2023 (09:49:56 CEST)

A peer-reviewed article of this Preprint also exists.

He, J.; Yang, L.; Chang, P.; Yang, S.; Wang, Y.; Lin, S.; Tang, Q.; Zhang, Y. Zika Virus Induces Degradation of the Numb Protein Required through Embryonic Neurogenesis. Viruses 2023, 15, 1258. He, J.; Yang, L.; Chang, P.; Yang, S.; Wang, Y.; Lin, S.; Tang, Q.; Zhang, Y. Zika Virus Induces Degradation of the Numb Protein Required through Embryonic Neurogenesis. Viruses 2023, 15, 1258.

Abstract

Zika virus (ZIKV) is a mosquito-borne flavivirus and causes an infection that is associated with neurological manifestations, including microcephaly and Guillain-Barre syndrome. The mechanism of ZIKV-mediated neuropathogenesis is not well understood. In this study, we discovered that ZIKV induces the degradation of the Numb protein, which plays a crucial role in neurogenesis by allowing asymmetric cell division during embryonic development. Our data show that ZIKV reduced the Numb protein level in a time- and dose-dependent manner. However, ZIKV infection appears to have minimal effect on the Numb transcript. Treatment of ZIKV-infected cells with a proteasome inhibitor restores the Numb protein level, which suggests the involvement of the ubiquitin-proteasome pathway. In addition, ZIKV infection shortens the half-life of the Numb protein. Among the ZIKV proteins, the capsid protein significantly reduces the Numb protein level. Immunoprecipitation of the Numb protein co-precipitates the capsid protein, indicating the interaction between these two proteins. These results provide insights into the ZIKV-cell interaction that might contribute to its impact on neurogenesis.

Keywords

Zika virus; ZIKV; the Numb protein; the Capsid protein

Subject

Biology and Life Sciences, Virology

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