The DC CFAR would like to congratulate Dr. Mark Burke, PhD, Assistant Professor in the Department of Physiology and Biophysics at Howard University, for his recent publication in ACS Chemical Nueroscience. The article, titled "Of Mice and Monkeys: Can animal models be utilized to study neurological consequences of pediatric HIV-1 infection", was a result of his DC CFAR Pilot Award on altered neurodevelopment in pediatric HIV infection. Dr. Burke's abstract can be found below.
Pediatric human immunodeficiency virus (HIV-1) infection remains a global health crisis. Children are much more susceptible to HIV-1 neurological impairments than adults, which can be exacerbated by co-infections. Neurological characteristics of pediatric HIV-1 infection suggest dysfunction in the frontal cortex as well as the hippocampus; limited MRI data indicate global cerebral atrophy, and pathological data suggest accelerated neuronal apoptosis in the cortex. An obstacle to pediatric HIV-1 research is a human representative model system. Host-species specificity of HIV-1 limits the ability to model neurological consequences of pediatric HIV-1 infection in animals. Several models have been proposed including neonatal intracranial injections of HIV-1 viral proteins in rats and perinatal simian immunodeficiency virus (SIV) infection of infant macaques. Non-human primate models recapitulate the complexity of pediatric HIV-1 neuropathogenesis while rodent models are able to elucidate the role specific viral proteins exert on neurodevelopment. Non-human primate models show similar behavioural and neuropathological characteristics to pediatric HIV-1 infection and offer a stage to investigate early viral mechanisms, latency reservoirs, and therapeutic interventions. Here we review the relative strengths and limitations of pediatric HIV-1 model systems.