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Abstract
The purpose of this study is to determine the effect of the Human Immunodeficiency virus (HIV) in producing neuropathic pain in an Alzheimer’s Disease (AD) mouse model. HIV-1 envelope glycoprotein gp120 is correlated with increased release of thermal hyperalgesia and mechanical allodynia mediators from astrocytes and glial cells in rodents, producing the identifiable symptoms of neuropathic pain. Similarly, studies show that 45.8% of AD patients experience chronic pain. The production of an HIV/AD comorbid mouse model will be useful in determining important pathological pathways for neuropathic pain and is vital to future studies in therapeutic approaches to these conditions. Two AD mouse models were used in this experiment: a humanized amyloid knock-in mouse (hAβKI, amyloidogenesis) (KI) and a human Tau P301L mutation (Tau) mouse. The chimeric HIV model was produced via peritoneal injection of species-specific EcoHIV (Eco) infections into mice.
Four groups of mice were tested using the Acetone and Von Frey methods for determining mechanical allodynia and thermal hyperalgesia levels: wild-type, wild-type + EcoHIV, hAβ (KI) + EcoHIV and Tau + EcoHIV. Each sample group’s responses were compared internally. Baseline pain responses were recorded before administration of the virus. The pain response testing was then repeated 4 weeks after the administration of the EcoHIV virus and the results compared for effectiveness in animal pain production. Thermal hyperalgesia responses were determined via application of acetone to the left rear paw of each mouse experimental group and observation of the time during which the mouse demonstrated temperature sensitivity behaviors. Mechanical allodynia was determined via pressure tolerance testing on the left rear paw using a von Fret aesthesiometer.
The results of this study demonstrate significant increases in mechanical allodynia and thermal hyperalgesia following the injection of EcoHIV in AD mouse models. A two-way ANOVA was performed to analyze the effect of the EcoHIV injection on the thermal hyperalgesia response in seconds. A statistically significant interaction between the effects of the injection and the experimental group (F (3, 118) = 175.9, p< 0.0001) was observed, as well as significant increases in thermal hyperalgesia (p< 0.0001). The same analysis was performed to analyze the effect on the paw-withdrawal threshold. A statistically significant interaction between the effects of the injection and experimental group (F(3,118) = 19.27, p< 0.0001) was observed, with significant effects on paw-withdrawal threshold (p< 0.0001). Thus, increased cold sensitivity and a decreased paw-withdrawal threshold was observed in all experimental groups administered EcoHIV, indicating the presence of neuropathic pain. The production of this HIV/AD neuropathic pain model has implications for medical research, providing a novel model mimicking human comorbid pathologies and offers insights into potential associations between AD and HIV neuropathic pain development. Future research within this project will determine the efficacy of Cannabidiol and beta-caryophyllene combined treatment for neuropathic pain in the produced HIV/AD mouse model.
Presentation Type
Poster
Recommended Citation
Usman, Ayesha; Szobody, Megan W.; Rios, Jose; Alnoud, Mohammed; and Benamar, Khalid, "Determining the effects of an HIV infective model on the development of neuropathic pain in Alzheimer’s Disease model mice." (2025). Research Colloquium. 68.
https://scholarworks.utrgv.edu/colloquium/2025/posters/68
Included in
Medical Anatomy Commons, Medical Neurobiology Commons, Medical Physiology Commons, Neurology Commons
Determining the effects of an HIV infective model on the development of neuropathic pain in Alzheimer’s Disease model mice.
The purpose of this study is to determine the effect of the Human Immunodeficiency virus (HIV) in producing neuropathic pain in an Alzheimer’s Disease (AD) mouse model. HIV-1 envelope glycoprotein gp120 is correlated with increased release of thermal hyperalgesia and mechanical allodynia mediators from astrocytes and glial cells in rodents, producing the identifiable symptoms of neuropathic pain. Similarly, studies show that 45.8% of AD patients experience chronic pain. The production of an HIV/AD comorbid mouse model will be useful in determining important pathological pathways for neuropathic pain and is vital to future studies in therapeutic approaches to these conditions. Two AD mouse models were used in this experiment: a humanized amyloid knock-in mouse (hAβKI, amyloidogenesis) (KI) and a human Tau P301L mutation (Tau) mouse. The chimeric HIV model was produced via peritoneal injection of species-specific EcoHIV (Eco) infections into mice.
Four groups of mice were tested using the Acetone and Von Frey methods for determining mechanical allodynia and thermal hyperalgesia levels: wild-type, wild-type + EcoHIV, hAβ (KI) + EcoHIV and Tau + EcoHIV. Each sample group’s responses were compared internally. Baseline pain responses were recorded before administration of the virus. The pain response testing was then repeated 4 weeks after the administration of the EcoHIV virus and the results compared for effectiveness in animal pain production. Thermal hyperalgesia responses were determined via application of acetone to the left rear paw of each mouse experimental group and observation of the time during which the mouse demonstrated temperature sensitivity behaviors. Mechanical allodynia was determined via pressure tolerance testing on the left rear paw using a von Fret aesthesiometer.
The results of this study demonstrate significant increases in mechanical allodynia and thermal hyperalgesia following the injection of EcoHIV in AD mouse models. A two-way ANOVA was performed to analyze the effect of the EcoHIV injection on the thermal hyperalgesia response in seconds. A statistically significant interaction between the effects of the injection and the experimental group (F (3, 118) = 175.9, p< 0.0001) was observed, as well as significant increases in thermal hyperalgesia (p< 0.0001). The same analysis was performed to analyze the effect on the paw-withdrawal threshold. A statistically significant interaction between the effects of the injection and experimental group (F(3,118) = 19.27, p< 0.0001) was observed, with significant effects on paw-withdrawal threshold (p< 0.0001). Thus, increased cold sensitivity and a decreased paw-withdrawal threshold was observed in all experimental groups administered EcoHIV, indicating the presence of neuropathic pain. The production of this HIV/AD neuropathic pain model has implications for medical research, providing a novel model mimicking human comorbid pathologies and offers insights into potential associations between AD and HIV neuropathic pain development. Future research within this project will determine the efficacy of Cannabidiol and beta-caryophyllene combined treatment for neuropathic pain in the produced HIV/AD mouse model.
