3.4.2 Regulation of ZIKV proteins on apoptosis
Newly results indicate that ZIKV-C protein interacts with
mouse double-minute-2 homolog
(MDM2), which is involved in the p53-mediated apoptosis pathway,
activating the death of infected neural
cells(Teng et al., 2017). Further
studies have shown that the nuclear localization of ZIKA-C is related to
ribosomal stress (RS) and
apoptosis, and the 22 C-terminal residues of ZIKV-C are essential for
nuclear localization, RS and
apoptosis(Slomnicki et al., 2017).
Moreover, DENV2-C was found to have a similar apoptosis-inducing
mechanism with ZIKA-C. ZIKV-prM protein can induce apoptotic cell death,
and the Pr region located on the N-terminal side of prM protein is
responsible for prM-induced apoptosis(G.
Li et al., 2019). In addition, E protein of ZIKV can induce apoptosis
in differentiating hNSC(Bhagat et al.,
2018). ZIKV-E can also inhibit the proliferation of PC12 cells,
triggere G2/M cell cycle arrest and apoptosis, further analysis showed
that ZIKV-E caused apoptosis via intrinsic cell death pathway that was
dependent on caspase-9/3 activation and accompanied by an increase in
the ratio of Bax to Bcl-2(J. Liu et al.,
2018).