Abstract
We describe current research that applies epigenetics to a novel understanding of the immuno-neuropathogenesis of HIV-1 viral infection and NeuroAIDS. We propose the hypothesis that HIV-1 alters the structure-function relationship of chromatin, coding DNA and non-coding DNA, including RNA transcribed from these regions resulting in pathogenesis in AIDS, drug abuse, and NeuroAIDS. We discuss the general implications of molecular epigenetics with special emphasis on drug abuse, bar-codes, pyknons, and miRNAs for translational and clinical research. We discuss the application of the recent recursive algorithm of biology to this field and propose to synthesize the Genomic and Epigenomic views into a holistic approach of HoloGenomics.
Highlights
In the era of highly active antiretroviral therapy (HAART) many factors, including host genetics, HIV strain variation, and comorbidities, including drug abuse and co-infection with hepatitis C virus (HCV) contribute to the pathogenesis of AIDS and NeuroAIDS [1, 2, 3]
We describe current research that applies epigenetics to a novel understanding of the immuno-neuropathogenesis of HIV-1 viral infection and NeuroAIDS
We propose the hypothesis that HIV-1 alters the structure-function relationship of chromatin, coding DNA and non-coding DNA, including RNA transcribed from these regions resulting in pathogenesis in AIDS, drug abuse, and NeuroAIDS
Summary
In the era of highly active antiretroviral therapy (HAART) many factors, including host genetics, HIV strain variation, and comorbidities, including drug abuse and co-infection with hepatitis C virus (HCV) contribute to the pathogenesis of AIDS and NeuroAIDS [1, 2, 3]. We propose the hypothesis that HIV-1 alters the structure-function relationship of chromatin, coding DNA and non-coding DNA, including RNA transcribed from these regions resulting in pathogenesis in AIDS, drug abuse, and NeuroAIDS.
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