TABLE 2.
Transcription factors activated by viruses
| Virus | Transcription factors |
|---|---|
| HSV | NF-κB, AP-1, ATF/CREB,a Oct-1b |
| CMV | NF-κB, AP-1, ATF/CREB, IRF-3 |
| EBV | NF-κB, AP-1, ATF-2/c-Jun, IRF-7 |
| Influenza virus | NF-κB, AP-1, ATF/CRE |
| HBV | NF-κB, AP-1, AP-2, ATF/CREB, Egr-1, C/EBPα, NF-AT, basal transcription factorsc |
| HIV | NF-κB, AP-1, Sp1,d GR,d C/EBPβ, NF-AT |
| HTLV-1 | NF-κB, AP-1, ATF-2, CREB-2,e C/EBPβe, NF-AT, Spi-1,e GBPe |
a
The specific nature of the CRE-binding proteins has not been determined.
b
Oct-1 activates immediate-early HSV promoters through interaction with VP16 and host cell factor.
c
The HBx protein promotes formation of the transcriptional initiation complex by interacting with the basal transcription factors TFIIB, TFIIIB and TATA-binding protein, as well as RNA polymerase II.
d
The HIV Vpr protein enhances the activity of Sp1 and GR by physical interaction.
e
Protein-protein interactions with Tax augment the activity of CREB-2, C/EBPβ, Spi-1, and GBP.