• Su-Bo Yuan, Yuqiang Shi, Jinghong Chen, Xiangfu Zhou, Guangyu Li, Benjamin B Gelman, Joshua G Lisinicchia, Susan M Carlton, Monique R Ferguson, Alai Tan, Sushil K Sarna, and Shao-Jun Tang.
• Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX.
• Ann. Neurol. 2014 Jun 1;75(6):837-50.

ObjectiveChronic pain is a common neurological comorbidity of human immunodeficiency virus (HIV)-1 infection, but the etiological cause remains elusive. The objective of this study was to identify the HIV-1 causal factor that critically contributes to the pathogenesis of HIV-associated pain.MethodsWe first compared the levels of HIV-1 proteins in postmortem tissues of the spinal cord dorsal horn (SDH) from HIV-1/acquired immunodeficiency syndrome patients who developed chronic pain (pain-positive HIV-1 patients) and HIV-1 patients who did not develop chronic pain (pain-negative HIV-1 patients). Then we used the HIV-1 protein that was specifically increased in the pain-positive patients to generate mouse models. Finally, we performed comparative analyses on the pathological changes in the models and the HIV-1 patients.ResultsWe found that HIV-1 gp120 was significantly higher in pain-positive HIV-1 patients (vs pain-negative HIV-1 patients). This finding suggested that gp120 was a potential causal factor of the HIV-associated pain. To test this hypothesis, we used a mouse model generated by intrathecal injection of gp120 and compared the pathologies of the model and the pain-positive human HIV-1 patients. The results showed that the mouse model and pain-positive human HIV-1 patients developed extensive similarities in their pathological phenotypes, including pain behaviors, peripheral neuropathy, glial reactivation, synapse degeneration, and aberrant activation of pain-related signaling pathways in the SDH.InterpretationOur findings suggest that gp120 may critically contribute to the pathogenesis of HIV-associated pain.© 2014 American Neurological Association.

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