Effects of Antiretroviral Drugs on Osteoclast Differentiation and Function
Session Number
2
Advisor(s)
Dr. Jennillee Wallace, Rush University
Location
A121
Discipline
Medical and Health Sciences
Start Date
15-4-2026 11:10 AM
End Date
15-4-2026 11:55 AM
Abstract
Antiretroviral drugs have significantly improved treatment outcomes for people living with HIV. However, long-term exposure to certain antiretroviral therapies (ARTs) has been associated with detrimental effects on bone metabolism. Our objective is to investigate how exactly the exposure to commonly used antiretroviral drugs influences osteoclast activity. CD14+ monocytes were isolated from human blood and then differentiated into mature osteoclasts. These cells were then treated with both individual and combination drugs, including tenofovir alafenamide (TAF), bictegravir (BIK), biktarvy (B), emtricitabine (FTC), and dimethyl sulfoxide (DMSO) as the vehicle control. Following treatment, bone samples were examined using DAPI nuclear staining, and osteoclasts were quantified by counting cells with three or more nuclei. Additional observations were used to evaluate maturation and resorptive activity, as well as potential cellular stress associated with ART exposure; this included mitochondrial dysfunction, which was evaluated via Seahorse XFe14 mitochondrial stress test. Ongoing and future studies will further characterize osteoclast function under ARTs.
Effects of Antiretroviral Drugs on Osteoclast Differentiation and Function
A121
Antiretroviral drugs have significantly improved treatment outcomes for people living with HIV. However, long-term exposure to certain antiretroviral therapies (ARTs) has been associated with detrimental effects on bone metabolism. Our objective is to investigate how exactly the exposure to commonly used antiretroviral drugs influences osteoclast activity. CD14+ monocytes were isolated from human blood and then differentiated into mature osteoclasts. These cells were then treated with both individual and combination drugs, including tenofovir alafenamide (TAF), bictegravir (BIK), biktarvy (B), emtricitabine (FTC), and dimethyl sulfoxide (DMSO) as the vehicle control. Following treatment, bone samples were examined using DAPI nuclear staining, and osteoclasts were quantified by counting cells with three or more nuclei. Additional observations were used to evaluate maturation and resorptive activity, as well as potential cellular stress associated with ART exposure; this included mitochondrial dysfunction, which was evaluated via Seahorse XFe14 mitochondrial stress test. Ongoing and future studies will further characterize osteoclast function under ARTs.