Table 1.

Host microRNA (miRNA) deregulated in herpes simplex virus 1 (HSV-1) infection and their targets.

miRNA	Up-/Downregulated	Target	Possible Roles	Model	References	Cellular Process
miR-23a	Down- then Upregulated	IRF1	Inhibition of innate immune response and cell survival	HeLa	[66]		APOPTOSIS
miR-649	Downregulated	MALT1	Inhibition of innate and adaptive immune response	HeLa	[78]
miR-101	Upregulated	ATP5B	Blocking DNA packaging and capsid maturation	HeLa	[79]	INHIBITION OF VIRAL REPLICATION
	Upregulated	GRSF1	Inhibition of viral protein synthesis	HeLa	[80]
miR-132	Upregulated	Ras-GAP	Immuno-inflammatory response leading to neovascularization and stromal keratitis lesions	Murine corneas	[81]	ANTIVIRAL IMMUNITY
	Upregulated	p300	Inhibition of innate immune response	Monocytes (THP-1 cell line)	[82]
miR-146a	Upregulated	Complement factor H	Evasion of HSV-1 from the innate immune response	Human neuronal-glial cells	[83]
miR-373	Upregulated	IRF1	Inhibition of innate immune response	HeLa and patients with herpetic gingivostomatitis	[74]
miR-155	Deficiency	SOCS1	Regulation of T cell differentiation	In vivo mouse model of herpes simplex encephalitis	[84]
	Upregulated	Unknown	-	In vivo acute viral encephalitis model—mouse brain	[85]	TARGET NOT KNOWN
miR-183/96/182	Upregulated	Unknown	-	Primary fibroblasts and neurons	[86]
miR-15b, miR-26a, miR-141, miR-183/96/182, miR-200a, b, c, miR-429 1	Upregulated	Unknown	-	In vivo acute viral encephalitis model—mouse brain	[85]

¹ All of these miRNAs are shown to be upregulated during HSV-1 infection, and syndecan-2 (Sdc2) has been shown to be a possible cellular target regulated by miR-96, miR-141, miR-183, and miR-200c.