| It is widely known that human immunodeficiency virus type-1 (HIV-1) can cause acquired immune deficiency syndrome (AIDS), but treatments to prevent the virus from escalating to that severity have come a long way since the virus was first described in the 1980s. The medications, combined antiretroviral therapy (cART), keep the virus from replicating, thus stopping its progression to AIDS. However, this treatment does not seem to ultimately benefit the brain, in part because cART does not uniformly penetrate the blood-brain barrier (BBB), and in part because HIV-1 seems to permanently turn on the part of the immune system that causes neuroinflammation. This allows the virus to exist in white blood cells and brain-resident glia amongst the neurons, wreaking havoc on the body's central nervous system (CNS). Harris Gelbard and his research laboratory aim to understand the molecules and pathways involved in neuroinflammation caused by HIV-1 and the resulting HIV-associated neurocognitive disorders (HAND). The lab's research has revealed several of the key components of this disease's progression and has even synthesized small molecules with drug-like properties that confer neuroprotection in models of HAND. Applications of these molecules in a pharmaceutical setting and its delivery method for humans have yet to be established. The artwork created for this Thesis will visualize some of the research through illustrations, an animation, and an interactive game. The artwork will be effective in communicating the complexity of the research with graphical representations due to the collaboration with and contributions from the members of the Gelbard laboratory. |
