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] |