Table 3.

The TRFs c-Rel and Oct-1 are functional during HSV infection

Tissue type	HSV strain	Oct-1	c-Rel	Function	Ref.
Kidney: Vero cells	HSV-1 strain 17	–	c-Rel	As a novel cause of HSE disease susceptibility.	[31]
Hematological: Jurkat cells	HSV-1	–	p65/c-Rel	the p65/c-Rel heterodimer is responsible for the NF-kB-dependent induction of HIV-1 LTR in HSV- 1-infected cells.	[32]
Embryonic: WT and dOct MEF cells	HSV-1 strain F	Oct-1	–	Oct-1 is required for the formation of HSV replication factories and late gene expression.	[33]
Digestive: Hep2 cells	HSV-1 strain KOS	Oct-1	–	Oct-1 directly recognizes TAATGARAT elements in promoters of IE genes.	[34]
Urinary: COS-7 cells	HSV-1 strain KOS	Oct-1	–	Distinct conformations of Oct-1 on the BHV IE1 sites and on the HSV IE110 sites.	[35]
Genital: HeLa cells	HSV-1 strain F	Oct-1	–	late in infection Oct-1 is posttranslationally modified and exhibits a reduced capacity to bind to its cognate sites.	[36]
Genital: HeLa cells	HSV-1 strain KOS	Oct-1	–	Ser375 is important for the interaction of VP16 with Oct-1, and that the interaction is required to enable both proteins to bind to IE promoters.	[28]
Genital: HFF	HSV-1 strain KOS	Oct-1	–	forms a transactivation complex with the cellular proteins HCF-1 and HSV-1 VP16 tegument protein.	[29]
Genital: HeLa cells	HSV-2 strain 333	Oct-1	–	the HSV-2 protein forms a transcriptional complex with the cellular Oct-1 protein and target TAATGARAT elements from immediate-early promoters.	[37]

HSE Herpes simplex encephalitis, HIV human immunodeficiency virus, LTR long terminal repeat