Distinct promoter activation mechanisms modulate noise-driven HIV gene expression.

ABSTRACT: Latent human immunodeficiency virus (HIV) infections occur when the virus occupies a transcriptionally silent but reversible state, presenting a major obstacle to cure. There is experimental evidence that random fluctuations in gene expression, when coupled to the strong positive feedback encoded by the HIV genetic circuit, act as a 'molecular switch' controlling cell fate, i.e., viral replication versus latency. Here, we implemented a stochastic computational modeling approach to explore how different promoter activation mechanisms in the presence of positive feedback would affect noise-driven activation from latency. We modeled the HIV promoter as existing in one, two, or three states that are representative of increasingly complex mechanisms of promoter repression underlying latency. We

SUBMITTER: Chavali AK 

PROVIDER: S-EPMC4678399 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature