Gp120 in the pathogenesis of human immunodeficiency virus–associated pain. Issue 6 (28th May 2014)

• Record Type: Journal Article
• Authors: Yuan, Su‐Bo; Shi, Yuqiang; Chen, Jinghong; Zhou, Xiangfu; Li, Guangyu; Gelman, Benjamin B.; Lisinicchia, Joshua G.; Carlton, Susan M.; Ferguson, Monique R.; Tan, Alai; Sarna, Sushil K.; Tang, Shao‐Jun
• Is Part Of: Annals of neurology. Volume 75:Issue 6(2014:Jun.)
• Page Start: 837
• Page End: 850
• Publication Date: 2014-05-28
• Subjects: Neurology -- Periodicals; Pediatric neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; 616.8
• DOI: 10.1002/ana.24139
• Languages: English
• ISSNs: 0364-5134

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="ana24139-sec-0001" sec-type="section"> <title>Objective</title> <p>Chronic 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.</p> </sec> <sec id="ana24139-sec-0002" sec-type="section"> <title>Methods</title> <p>We 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.</p> </sec> <sec id="ana24139-sec-0003" sec-type="section"> <title>Results</title> <p>We 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.</p> </sec> <sec id="ana24139-sec-0004" sec-type="section"> <title>Interpretation</title> <p>Our findings suggest that gp120 may critically contribute to the pathogenesis of HIV‐associated pain. Ann Neurol 2014;75:837–850</p> </sec> </abstract>