E-mail: Tuskegee University
Department: Integrated Biosciences
Advisor: Deloris Alexander
Captopril and calcium carbonate nanoparticles as novel therapeutic strategies for the treatment of HSV-1 infection
According to Xu et al. (2006), it is estimated that approximately 60% of Americans are infected with Herpes Simplex Virus Type I (HSV-1) and that number is expected to be even greater worldwide. HSV-1 is continually documented as being a leading infectious cause of acute, sporadic encephalitis, corneal blindness (Webre et al., 2011) and the leading cause of viral encephalitis. This project focuses on examining interactions between HSV-1, Captopril and Calcium nanoparticles and how the Captopril and Calcium nanoparticles may be able to reduce detrimental effects induced by HSV-1 infection. Moreover, this project will focus on the efficacy of Captopril and Calcium carbonate loaded nanoparticles as therapeutic agents against the detrimental effects induced by HSV-1 infection. The effects of HSV-1 infection and reactivation appear to be substantial clinical problems, yet there is not a sufficient amount of research addressing these specific problematic areas. The ability to better understand the mechanisms inhibiting infection and reactivation from latency may provide insight into therapeutic alternatives capable of preventing infection. Antiviral agents can be used to treat disease, to prevent infection, or to prevent disease. The majority of antiviral medications with activity against HSV-1 are nucleoside analogues; the efficacy of these medications are often limited by the development an antiviral resistance (Kimberlain, 2007). Various HSV-1 induced pathologies and the lack of effective treatment create a dire need for finding novel antiviral targets. Novel antiviral targets include Renin Angiotensin System (RAS) components, HSV-1 genome, and nanoparticles. RAS is a hormonal cascade functioning primarily to maintain homeostatic control of arterial and osmotic pressure. In addition to its well known function, previous research suggests RAS components may have some concentration dependent anti-viral effects. Thus, we have preliminarily tested the hypothesis that Captopril attenuates cytopathic effects of HSV-1 in SH-SY5Y neuroblastoma cells. Cell viability data gathered from trypan blue and MTT assays demonstrate a dose-dependent protection of cells by Captopril. Based off experimental results, captopril and components of the RAS may prove to be effective therapeutic targets in reducing neurological insults prompted by HSV-1 infection.