Table 1.

Viral infections induced HERVs transactivation

Viruses	HERV family	Possible mechanisms	Ref.
HSV-1	W, K	IE1 stimulates LTR of HERV-W trough enhancing the activity of Oct-1; ICP0 increases transcription LTR of HERV-K through AP-1 site.	36, 42, 43
VZV	Unknown	VZV can sustain the increase in the RT expression.	89
HCMV	T, W, F, K, L	HCMV-induced cytokines and growth factors may enhance HERV activation.	68, 69
EBV	W, K	LAM-2A and LMP-1 activate HERV-K in infected B lymphocytes; EBV infection activates HERV-K in resting B lymphocytes through binding CD21; HERV-W activation was regulated by EBV gp350 in PBMC.	37, 57– 59, 90
HHV-6	K	HHV-6A induces HERV-K18-encoded superantigen through IFN-α; HHV-6B induced superantigen HERV-K18, which may have consequences for the development of autoimmunity.	91, 92
KSHV	K	LANA induces env transcripts through enhancing ERK activity; vFLIP induces env transcripts through activating NF-κB activity.	33
HIV-1	K, E, W, T	HERV-K (HML-2) is activated by Tat through regulating NF-κB and NF-AT.	2, 32, 40
HTLV-1	K, E, W, H	Tax is able to activate HERV LTRs, mainly of HERV-W and -H.	35, 74
HBV	W	HBV X Protein induces overexpression of HERV-W env through NF-κB.	34
Influenza A virus	W	Influenza A virus infection can transactivate ERVWE1 by increasing the transcription of GCM1 and reducing the repressive histone mark H3K9me3.	36, 41