Table 1.

Summary of the main studies addressing TORCH pathogens’ effects on neural progenitor cells (NPCs), neural stem cells (NSCs), and their progeny. ER: endoplasmic reticulum.

Pathogen	Targets	Effects	Models	References
ZIKV	NPCs	AKT-mTORC pathway inhibition	Human fetal NSCs	[36]
		STING cleavage	Human fibroblasts	[37]
		SEPTIN2 cleavage	NPCs obtained from human H9 ESC-derived embryoid bodies	[38]
		Centrosomal aberration	Human neocortical NES cells	[23]
		pTBK1 relocation	Human neocortical NES cells	[23]
		Proliferation impairment	Human iPSC-derived forebrain organoids	[39,40]
		Radial scaffold disorganization and architectural impairment	Human organotypic fetal brain slices, post-mortem fetal brain samples	[23]
		Cell death	Human iPSC-derived forebrain organoids	[39,40]
	Neuronal progeny/Immune cells	Acute flaccid paralysis: (i) damage of motor neurons, (ii) Guillan–Barrè syndrome	/	[41]
		Meningoencephalitis	/	[42,43]
T. gondii	NPCs	Gliogenesis induction	Mouse NPCs	[44]
		Neurogenesis impairment	Mouse NPCs	[44]
		ER stress dependent apoptosis	Mouse NSCs	[45]
	Neuronal progeny	Apoptosis	/	[46]
		Neurotransmitter metabolism alteration	Neural cells in mouse brain tissue	[46,47]
		Neuroinflammation	/	[48,49,50]
		Synaptic modification	Mouse model	[46,51]
		Behavioral alterations and psychiatric diseases	Primary human temporal-lobe NSC lines	[46,52,53,54]
Rubella Virus	NPCs	Cell death	Autoptic fetal tissue	[55]
	Neuronal progeny	Cell death	Autoptic fetal tissue	[55,56,57]
CMV	NPCs	Neurogenesis impairment	Human iPSC-derived brain organoids	[58]
		Migration impairment	Human iPSC-derived brain organoids	[58]
		pTBK1 relocation	Human neocortical NES cells	[23]
		Proliferation impairment	Human fetal brain-derived NPCs; human fetal NES cells; hNPCs	[59,60,61]
		Cell death	Primary human neuronal cell cultures; human fetal NES cells; hNPCs; human iPSC-derived brain organoids	[58,59,61,62,63]
		Dysregulation of genes involved in multipotency, modulation of cellular excitability and calcium signaling	Human iPSC-derived NSCs; hNPCs; human iPSC-derived brain organoids	[58,64,65]
		SOX4, DCX, Nestin, SOX2 and GFAP proteasomal degradation	Human fetal brain-derived NPCs; hNPCs	[60,64]
	Neuronal progeny	Apoptosis	Human iPSC-derived NSCs	[65]
		Downregulation of NMDA receptor	Human iPSC-derived NSCs	[65]
HSV	NPCs	Proliferation surge (in acute phase)	Mouse NSCs	[66]
		Proliferation impairment (in chronic phase)	Mouse NSCs	[66]
		Neurogenesis impairment (in chronic phase)	Mouse NSCs	[66]
		APP fragmentation	Mouse adult hippocampal NSCs	[67]
		Gliogenesis induction	Mouse adult hippocampal NSCs	[67]
	Neuronal progeny	G1 re-entry stimulated apoptosis	Cerebellar granule cells; rat dorsal root ganglion neurons; human neuronal cell line; rat sympathetic neurons	[68,69,70,71]
		Golgi apparatus remodeling	Mouse cortical neurons	[72]
		Changes in architecture and functional activity	Human iPSC-derived neurons	[73]
		Decrease of synaptic transmission	Mouse cortical neurons	[74]
		Accumulation of APP fragments	Primary cultures of cortical neurons from rat embryos; mouse brains	[75,76,77]
		Increase of intracellular calcium	Rat cortical neurons	[77]
		Increase of Tau phosphorylation and cleavage	Mouse fetal neurons; AD brain specimens	[78,79]
		Neuroinflammation	Human brain organoids; mouse models	[80,81]
CoxB	NPCs	Cell death	Neonatal mice brain; mouse cortical NPCs	[82,83,84]
		Migration and neurogenesis impairment	Neonatal mice central nervous system	[85]