Infection with pH1N1 virus could promote HIV-1 RNA production by activating host transcription factors including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ĸB), nuclear factor of activated T-cells (NFAT) and activator protein 1 (AP-1) through mitogen-activated protein kinases (MAPK) pathways and T-cell antigen receptor (TCR)-related pathways.
The activation effect of NS3/4A to HIV-1 transcription can be explained by its ability to enhance DNA binding activities of the transcription factor AP-1.
Two promoters with the kB-site(s), those of human immunodeficiency virus (HIV) and SV40, were not activated by v-Rel, but their kB-sites were activated when introduced upstream of the c-jun promoter (-52/+148).
Interactions of the transcription factor AP-1 with the long terminal repeat of different human immunodeficiency virus type 1 strains in Jurkat, glial, and neuronal cells.