Associate Professor
Jacobs School of Medicine & Biomedical Sciences
Gene therapy; Genomics and proteomics; Immunology; Infectious Disease; Neurobiology; Neuropharmacology; Viral Pathogenesis; Virology
My research is dedicated to increasing knowledge on the interactions between the nervous and immune systems in the context of infectious disease and substance abuse disorders. My research investigates the neuroimmune mechanisms of infectious disease in relation to drugs of abuse, as it is well established that substance abuse disorders are inextricably linked with HIV/AIDS. Specifically, we explore the effects of cocaine and heroin on HIV-1 infectivity in dendritic cells, peripheral blood mononuclear cells, and astrocytes. We found that these drugs significantly upregulated HIV-1 replication in human astrocytes, dendritic cells, and peripheral blood mononuclear cells. We were one of the first laboratories to demonstrate these seminal findings in astrocytes. These findings confirmed the detrimental effects of drugs of abuse on HIV replication in immune and central nervous system cells. We also demonstrated that cocaine, heroin, and methamphetamine differentially regulate the expression of a number of proteins that may play a role in the neuropathogenesis of HIV-1 disease. These proteins are potential novel markers for diagnostic, preventive, and therapeutic targeting in drug-using individuals.
Additionally, I have a strong interest in the development of therapeutic delivery tools using nanomedicine to modulate both the nervous and immune systems. I have developed a body of work in nanomedicine, which is the medical application of nanotechnology and includes a wide range of applications. Towards this end I have been developing nanotechnology and biological based delivery vehicles that target astrocytes, microglial cells, and macrophages. These cells play a prominent role in HIV and neuroAIDs pathogenesis and co-infections associated with HIV such as tuberculosis (TB). My laboratory has developed a new therapy that combines anti-TB drugs with the actions of the innate immune system, to synergistically act to eradicate pathogens. This could potentially reduce the drug dosage required, shorten treatment duration, mitigate dose‐dependent toxicity, and reduce the emergence of drug resistance.