Table 1.

Interactions between pattern recognition receptors (PRRs) and viruses in astrocytes.

Receptor	Virus	Cell/Tissue	Direct and Indirect Effects of Viral Binding to PRRs	References
TLRs (2–4)	polyI:C	human astrocytes	upregulation of TLRs (2–4), secretion of IL-6 and CXCL-10, expression of IFN-β	[73]
TLR7	EV71	cerebral cortex in mice, mouse astrocytes	production of IL-6, apoptosis	[23]
TLR3, TLR4	ZIKV	human astrocytes	increase in the release of RANTES, IP-10, IFN-β, autophagy, TLR3, TLR4 expression	[10]
TLR3	WNV	mouse brain	encephalitis, breakdown of the blood–brain barrier	[74]
RIG-1, MDA-5	VSV, Sendai virus	mouse astrocytes	increase in the expression of RIG-1, MDA-5, release of IL-6, TNF-α	[27]
RIG-1, MDA-5	lab-attenuated RABV	mouse astrocytes	activation of MAVS, production of TNF-α, IFN-γ, IL-6, IL-1β, IL-17, VEGF,	[75]
TLR1-3	lab-attenuated RABV	mouse brain	IFNα/β signaling pathway stimulated expression of many genes encoding inflammatory molecules such as chemokines, cytokines, TLRs (TLR1–3), and complement components	[76]
TLR-dependent MyD88 signaling	TMEV	Mouse astrocytes	release of IFN-β	[63]
DC-SIGN	HIV-1	human astrocytes	Endocytosis of HIV-1	[77]

Table 1 delineates known interactions between pattern-recognition receptors (PRRs) and viruses in astrocytes. Note that interactions between NLRs and viruses are unexplored in astrocytes. poly(inosinic acid):poly(cytidylic acid) (polyI:C); human Enterovirus 71 (EV71); Japanese encephalitis virus (JEV); Zika virus (ZIKV), West Nile virus (WNV); vesicular stomatitis virus (VSV); lab-attenuated rabies virus strain (RABV), Theiler’s murine encephalomyelitis virus (TMEV), mitochondrial antiviral-signaling protein (MAVS), human immunodeficiency virus (HIV-1); myeloid differentiation primary response gene 88 (MyD88).