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Joan Smith Sonneborn

Joan Smith Sonneborn

University of Wyoming,USA.

Title: Novel drug reservoirs offer potential therapeutic intervention in HIV pathology

Biography

Joan Smith Sonneborn, a Professor Emeritus from the Zoology and Physiology Department at the University of Wyoming,  focuses on how  threshold levels of stress, including exercise stress,  can trigger beneficial rejuvenation and anti aging effects on the brain and body and disease intervention.  Intervention in aging and related diseases have been her passion especially using animal model systems’ strategies to tap into our natural reserves to tolerate challenges and preserve or activate energy systems. Association Certified trainer. She is an avid promoter of exercise, and enjoys both strength training and step class

Abstract

HIV infection shares fundamental stresses and abnormal gene function common to multiple disorders, i.e., cancer, Alzheimer’s, diabetes, neurological disorders, and ischemic shock.  HIV disease then, may benefit from other treatment drugs repurposed for HIV therapy.  The goal is to regulate master gene switches that promote stress tolerance.  Mimetics of stress can induce stress tolerance, and likewise can serve as HIV drugs. Telomerase is a master switch in cell life or death and for mitochondrial function in innate and adaptive immune functions. However, telomerase is inhibited by HIV proteins in specific cells.  Mitochondrial dysfunction directly modulates immune competence and energy availability. TERT dysfunction activates tumor suppressor p53 and the proapoptotic Bcl-2 protein Bax, destroys mitochondria, and induces Ipaf mRNA, a caspase 1 activator to promote HIV pathology. Studies show that activation of telomerase using (TAT2) induces antiviral activity in vitro. Likewise, genetic manipulation of telomerase in HIV-specific CD8+ T cells enhances antiviral function, increases proliferative potential and telomere length stabilization. Telomerase deficit is associated with HIV progression and telomerase upregulation in viral suppression, Given the paramount role of mitochondrial function in HIV tolerance, drugs that counteract oxidative stress, especially mitochondria targeted antioxidants, are candidate drugs both for HIV individuals without benefit of HIV standard therapy and/or as supplement to standard therapy. Nrf2 activators known to switch on antioxidant and stress resistant pathways, as well as anti-aging over the counter drugs, i.e., resveratrol, lipoic acid, and acetyl carnitine, are potental HIV therapy drugs, The alteration of sugar metabolism by mitochondrial dysfunction, implies a potential benefit of diabetic drugs repurpose for HIV infected individuals, Exercise and exercise mimetics induce master switches to tolerate stress, and thus offer HIV resistance therapy. Epigenetic drugs that alter methylation patterns have dose dependent HIV drug benefit potential