Table.

Current update and model systems used for zika virus infection in various brain cell types

Cell type	Efficiency	Effects	Model system	Pathways/molecules involved	References
NSCs	+++	Apoptosis, cell cycle arrest, inhibition of NSC differentiation, migration	In vivo mouse/human, in vitro mouse/human	CASP-3 activation, TLR3 signalling, autophagy, ER stress and UPR, dysregulation of mTOR signalling, mir-204-3p/PAX3 and mir-1273g-3p/NOTCH2 axis	21 55 60 62 72 73 77
Astrocytes	++	Activation, proliferation, apoptosis	In vivo mouse, in vitro human/mouse	UPR, autophagy	23 25 82
Microglia	+	Activation	In vitro mouse, in vivo mouse	IFNα signalling, proinflammatory molecules - IL-6, MCP1, TNFα, IL1β, IL8, MIP-1α, iNOS	25 72
Oligodendrocytes	+	Apoptosis	In vitro mouse	-	86
Brain microvascular endothelial cells	++	Activation, apoptosis	In vivo mouse in vitro human	IFNβ, IFNλ, interferon stimulated genes - IFIT1, ISG15, IFIT2, IL6, CCL5	87 88 89
Neurons-CNS	+	Apoptosis	In vivo human/mouse, in vitro human/mouse	CASP-3 activation	55 76
Neurons-PNS	++	Apoptosis	In vivo mouse, in vitro mouse	CASP-3 activation	77 80 81

+, ++, +++ depicts the degree of susceptibility of cells towards ZIKV. CNS, central nervous system; PNS, peripheral nervous system; NSC, neural stem cell; TLR3, toll-like receptors-3; UPR, unfolded protein response; CASP-3, Caspase-3