Characterization of rodent models of HIV-gp120 and anti-retroviral-associated neuropathic pain
Open accessAbstract
A distal symmetrical sensory peripheral neuropathy is frequently observed in people living with Human Immunodeficiency Virus Type 1 (HIV-1). This neuropathy can be associated with viral infection alone, probably involving a role for the envelope glycoprotein gp120; or a drug-induced toxic neuropathy associated with the use of nucleoside analogue reverse transcriptase inhibitors as a component of highly active anti-retroviral therapy. In order to elucidate the mechanisms underlying drug-induced neuropathy in the context of HIV infection, we have characterized pathological events in the peripheral and central nervous system following systemic treatment with the anti-retroviral agent, ddC (Zalcitabine) with or without the concomitant delivery of HIV-gp120 to the rat sciatic nerve (gp120+ddC). Systemic ddC treatment alone is associated with a persistent mechanical hypersensitivity (33% decrease in limb withdrawal threshold) that when combined with perineural HIV-gp120 is exacerbated (48% decrease in threshold) and both treatments result in thigmotactic (anxiety-like) behaviour. Immunohistochemical studies revealed little ddC-associated alteration in DRG phenotype, as compared with known changes following perineural HIV-gp120. However, the chemokine CCL2 is significantly expressed in the DRG of rats treated with perineural HIV-gp120 and/or ddC and there is a reduction in intraepidermal nerve fibre density, comparable to that seen in herpes zoster infection. Moreover, a spinal gliosis is apparent at times of peak behavioural sensitivity that is exacerbated in gp120+ddC as compared to either treatment alone. Treatment with the microglial inhibitor, minocycline, is associated with delayed onset of hypersensitivity to mechanical stimuli in the gp120+ddC model and reversal of some measures of thigmotaxis. Finally, the hypersensitivity to mechanical stimuli was sensitive to systemic treatment with gabapentin, morphine and the cannabinoid WIN 55,212-2, but not with amitriptyline. These data suggests that both neuropathic pain models display many features of HIV- and anti-retroviral-related peripheral neuropathy. They therefore merit further investigation for the elucidation of underlying mechanisms and may prove useful for preclinical assessment of drugs for the treatment of HIV-related peripheral neuropathic pain.
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Perineural HIV-gp120 together with zalcitabine treatment resulted in mechanical allodynia greater than either treatment alone, with no changes in paw withdrawal latencies to thermal stimuli or motor deficits.
“Perineural HIV-gp120 together with ddc treatment resulted in mechanical allodynia that was greater than either treatment alone; no changes in paw withdrawal latencies to thermal stimuli or motor deficits reported.123”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [123]
No hypersensitivity to thermal stimuli or motor deficits was observed following zalcitabine treatment.
“No hypersensitivity to thermal stimuli or motor deficits was observed following ddc treatment.”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [123]
Rats receiving zalcitabine displayed modest gliosis whereas combined treatment with HIV-gp120 and zalcitabine increased microglial activation.
“Rats receiving ddc displayed modest levels of gliosis whereas combined treatment with both HIV-gp120 and ddc increased levels of microglial activation.123”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [123]
Thigmotaxis was present in animals receiving zalcitabine, either alone or with HIV-gp120, indicating anxiety-like behavior.
“Thigmotaxis was present in animals receiving ddc, either alone or in conjunction with HIV-gp120, indicating the presence of anxiety-like behavior in these rats.123”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [123]
Rats treated with zalcitabine developed mechanical allodynia that persisted up to 43 days post-injection and peaked between days 14 and 32.
“Rats treated with the antiretroviral agent zalcitabine (ddc) developed mechanical allodynia that persisted up to 43 days post-injection and peaked between days 14 and 32.123”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [123]
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Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside
Rahn, E. J., & Hohmann, A. G. (2009) · Neurotherapeutics · doi:10.1016/j.nurt.2009.08.002 · Cited by 305 · see citing works
McAllister, S. L., McGinty, K. A., Resuehr, D., & Berkley, K. J. (2009) · Pain · doi:10.1016/j.pain.2009.09.022 · Cited by 59 · see citing works
- Authors
- Wallace, V. C. J., Blackbeard, J., Segerdahl, A. R., Hasnie, F., Pheby, T., McMahon, S. B., & Rice, A. S. C.
- Affiliations
- Chelsea and Westminster Hospital (GB)
- Guy's Hospital (GB)
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-10-01
- Volume
- 130
- Issue
- 10
- Pages
- 2688-2702
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC2656646
- OpenAlex
- W2134914347
- Cited by
- 176
- References
- 91
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 5 · 2023: 8 · 2022: 8 · 2021: 11 · 2020: 8 · 2019: 5 · 2018: 6 · 2017: 7 · 2016: 11 · 2015: 5 · 2014: 24 · 2013: 17 · 2012: 11
- FWCI
- 6.01
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Brain (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Pfizer
- Wellcome Trust (065374)
- Topics
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Health Sciences › Medicine › Oncology › Cancer Treatment and Pharmacology
- Health Sciences › Medicine › Infectious Diseases › HIV/AIDS drug development and treatment
- Keywords
- HIV-associated peripheral neuropathy, HIV gp120, zalcitabine, drug-induced neuropathy, nucleoside reverse transcriptase inhibitors, antiretroviral therapy, neuropathic pain, mechanical hypersensitivity, thigmotaxis, anxiety-like behavior, dorsal root ganglia, CCL2 chemokine, minocycline, gabapentin, WIN 55,212-2
- MeSH terms
- Animals, Anti-Bacterial Agents, Cold Temperature, Disease Models, Animal, Epidermis, Ganglia, Spinal, Gliosis, Hot Temperature, Hyperalgesia, Male, Minocycline, Motor Activity, Nerve Fibers, Nerve Tissue Proteins, Pain Measurement, Peripheral Nervous System Diseases, Physical Stimulation, HIV Envelope Protein gp120, Zalcitabine, Rats, Wistar, Pain Threshold, Reverse Transcriptase Inhibitors, Chemokine CCL2, Anti-HIV Agents, Rats
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