Because Dr. Kamel Khalili has been studying molecular neuropathogenesis of viral-induced diseases for over thirty years, he is extremely qualified to be speaking on the topic of HIV replication and gene editing therapy in the CBS news article In a first, scientists eliminate HIV from an animal’s genome. Aside from his dedication to the field, he is the director of the Comprehensive NeuroAIDS Center and co-director of the Center for Translational NeuroAIDS Researcher as well as the Director of the Center for Neurovirology at the Lewis Katz School of Medicine at Temple University. Not only do his credentials confirm his credibility, but also his important discoveries, such as the development of PML in the brain of AIDS patients among many others, further his qualifications. One of his many publications include his research paper titled Mitochondrial dysfunction in human immunodeficiency virus-1 transgenic mouse cardiac myocytes.
In this paper, Dr. Khalili describes his research and desire to find a cause and treatment for complications that occur as a result of chronic HIV-1 infection. In particular, he is trying to minimize the risk for cardiac dysfunction after infection of HIV-1. Although combination antiretroviral therapy has improved life expectancy and shifted the infection from a highly lethal one to a chronic disease, he seeks to understand the pathogenesis so that he can create an effective treatment for associated complications like cardiomyopathy. To do this, he and his colleagues used HIV-1 transgenic mice to see how HIV-related proteins affected myocyte function.
During a coimmunoprecipitation experiment, a physical association was made between BAG3 and an HIV protein, which led to the findings in their conclusion. By the end of the experiment, they found that the HIV-1 transgenic mice’s mitochondria were greatly affected and were not able to take in calcium. The research group concluded that under basal conditions, calcium uptake and ATP production by mitochondria was decreased in the transgenic mice’s myocytes. Along with this, oxygen levels were higher and contraction amplitudes were reduced, which was then able to be resolved with BAG3 overexpression after hypoxia/reoxygenation in the presence of isoproterenol. Unfortunately, the pathophysiology of HIV-associated cardiomyopathy is still unknown, despite the extensive research of this experiment.
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The research that Dr. Kamel Khalili has conducted is extremely important to people affected by HIV everywhere. Although there is a way to minimize the effects of HIV-1, this research can further the solution to lessen the symptoms and lingering effects of the disease even more. Due to extensive experience in the field and clear expertise demonstrated by both his numerous publications and his many leadership roles, Dr. Khalili is more than qualified to speak on matters related to HIV research.
