Sterol Regulatory Element-Binding Protein 2 Couples HIV-1 Transcription to Cholesterol Homeostasis and T Cell Activation

Caveolin-1 suppresses Human Immunodeficiency virus-1 replication by inhibiting acetylation of NF-κB

“…No. 632446, Clontech, Mountain View, CA) to generate LTR reporters as previously described (Taylor et al, 2011). The following primers were used to generate HIV-1-LTR and HIV-1-NF-κB mutant LTR reporters: wtLTR-Zsgreen- 5′-TGACATCGAGCTTGCTACAAGGGACTTTCCGCTGGGGACTTTCC-3′ and nkLTR-Zsgreen 5′-TGACATCGAGCTTGCTACAAGCCACTTTCCGCTGGGGACTTTCC-3′.…”

Biochemistry and biology of the inducible multifunctional transcription factor TFII-I: 10years later

“…A recent study remarkably shows a regulatory circuit involving TFII-I that is crucial for HIV-infection (Taylor et al, 2011). It is known that HIV-1 infection of CD4+ T cells activates genes involved in cholesterol homeostasis via sterol regulatory element-binding protein 2 (SREBP2).…”

“…Consistent with earlier studies, TFII-I expression is enhanced upon CD4+ T cell activation via TCR ligation regardless of HIV-1 infection. Therefore, these studies imply that apart from HIV-1 transcription, TFII-I regulates cholesterol homeostasis, although TFII-I responsive genes involved in this pathway have not yet been identified (Taylor et al, 2011). Another interesting extension from these studies is that TFII-I may also control interferon response in HIV-1 infected CD4+ T cells.…”

“…Microarray studies indicate that TFII-I potentially controls Interferon regulatory factor-7 (IRF-7) expression (Ashworth and Roy, 2009). Given that interferon response pathways are dysregulated upon HIV-1 infection, TFII-I might mediate interferon response during HIV-1 infection (Taylor et al, 2011). …”

Boots for Achilles: Progesterone's Reduction of Cholesterol Is a Second-Order Adaptation

“…Human cytomegalovirus has been shown to alter fatty acid biosynthesis pathways to increase fatty acid supply, which is essential for optimal viral growth (Munger et al 2008). West Nile virus acts similarly, modulating host cell cholesterol homeostasis by upregulating cholesterol biosynthesis and redistributing cholesterol to viral replication membranes (Mackenzie et al 2007); the same pattern has been shown in both Dengue virus (Heaton et al 2010) and HIV (Taylor et al 2011). It is thus quite likely that natural selection has favored host mechanisms that reduce or sequester cholesterol as a means of combating pathogens.…”