Gp120 in the pathogenesis of human immunodeficiency virus-associated pain

Su Bo Yuan, Yuqiang Shi, Jinghong Chen, Xiangfu Zhou, Guangyu Li, Benjamin Gelman, Joshua G. Lisinicchia, Susan M. Carlton, Monique Ferguson, Alai Tan, Sushil K. Sarna, Shao-Jun Tang

Research output: Contribution to journalArticle

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Abstract

Objective 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. Methods 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. Results 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. Interpretation Our findings suggest that gp120 may critically contribute to the pathogenesis of HIV-associated pain. Ann Neurol 2014;75:837-850

Original languageEnglish (US)
Pages (from-to)837-850
Number of pages14
JournalAnnals of Neurology
Volume75
Issue number6
DOIs
StatePublished - 2014

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HIV-1
HIV
Pain
Chronic Pain
Human Immunodeficiency Virus Proteins
Spinal Injections
Peripheral Nervous System Diseases
Virus Diseases
Neuroglia
Synapses
Comorbidity
Acquired Immunodeficiency Syndrome
Pathology
Phenotype

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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Gp120 in the pathogenesis of human immunodeficiency virus-associated pain. / Yuan, Su Bo; Shi, Yuqiang; Chen, Jinghong; Zhou, Xiangfu; Li, Guangyu; Gelman, Benjamin; Lisinicchia, Joshua G.; Carlton, Susan M.; Ferguson, Monique; Tan, Alai; Sarna, Sushil K.; Tang, Shao-Jun.

In: Annals of Neurology, Vol. 75, No. 6, 2014, p. 837-850.

Research output: Contribution to journalArticle

Yuan, SB, Shi, Y, Chen, J, Zhou, X, Li, G, Gelman, B, Lisinicchia, JG, Carlton, SM, Ferguson, M, Tan, A, Sarna, SK & Tang, S-J 2014, 'Gp120 in the pathogenesis of human immunodeficiency virus-associated pain', Annals of Neurology, vol. 75, no. 6, pp. 837-850. https://doi.org/10.1002/ana.24139
Yuan, Su Bo ; Shi, Yuqiang ; Chen, Jinghong ; Zhou, Xiangfu ; Li, Guangyu ; Gelman, Benjamin ; Lisinicchia, Joshua G. ; Carlton, Susan M. ; Ferguson, Monique ; Tan, Alai ; Sarna, Sushil K. ; Tang, Shao-Jun. / Gp120 in the pathogenesis of human immunodeficiency virus-associated pain. In: Annals of Neurology. 2014 ; Vol. 75, No. 6. pp. 837-850.
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N2 - Objective 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. Methods 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. Results 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. Interpretation Our findings suggest that gp120 may critically contribute to the pathogenesis of HIV-associated pain. Ann Neurol 2014;75:837-850

AB - Objective 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. Methods 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. Results 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. Interpretation Our findings suggest that gp120 may critically contribute to the pathogenesis of HIV-associated pain. Ann Neurol 2014;75:837-850

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