Comorbid Pain Syndromes in HIV-Associated Peripheral Neuropathy

Navis, Allison; Jiao, Jocelyn; George, Mary Catherine; Simpson, David M.; Robinson‐Papp, Jessica

doi:10.1093/pm/pnx129

Cited by 20 publications

(13 citation statements)

References 20 publications

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“…Human immunodeficiency virus-associated sensory neuropathy (HIV-SN) continues to be a frequent and challenging neurologic complication of HIV infection despite widespread use of modern combination antiretroviral therapy (cART) (1)(2)(3)(4). Patients with HIV-SN typically present with numbness, parestethias, and pain most severely affecting the distal extremities (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

SIV-Induced Immune Activation and Metabolic Alterations in the Dorsal Root Ganglia During Acute Infection

Mangus¹,

Weinberg²,

Knight³

et al. 2018

Journal of Neuropathology &Amp; Experimental Neurology

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Human immunodeficiency virus-associated sensory neuropathy (HIV-SN) remains a frequent neurologic complication of HIV infection. Little is known about alterations in the peripheral nervous system during the early stages of HIV, a time when neuroprotective interventions may be most beneficial. We performed Nanostring gene expression analysis on lumbar dorsal root ganglia (DRG) from 6 simian immunodeficiency virus (SIV)-infected pigtailed macaques killed at 7 days post-inoculation and 8 uninfected controls. We found significant upregulation of many genes involved in immune signaling and activation in the DRG. Among genes related to glutamate metabolism, there was significant upregulation of glutamine synthetase (GS), while glutaminase (GLS) was downregulated. Several genes involved in the oxidative stress response also showed significant differential regulation in the DRG of 7d SIV-infected animals, with superoxide dismutase-2 (SOD2) showing the greatest median fold change compared to controls. Novel findings in the DRG were compared to corresponding brain data and further investigated at the protein level by Western blotting and immunohistochemistry. Together with our previous finding of significant epidermal nerve fiber loss at 14 days post-SIV infection, results of this study demonstrate that immune activation and altered cellular metabolism at in the DRG precede and likely contribute to early sensory nerve injury in HIV-SN.

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Section: Introductionmentioning

confidence: 99%

SIV-Induced Immune Activation and Metabolic Alterations in the Dorsal Root Ganglia During Acute Infection

Mangus¹,

Weinberg²,

Knight³

et al. 2018

Journal of Neuropathology &Amp; Experimental Neurology

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“…Considering the limitation of the questionnaire or self-report data, it is difficult to distinguish whether chronic pain is due to pathogen, neuropathy, or just cART induced. Additionally, patients with HIV-associated neuropathy are more than twice as likely to have other chronic pain disorders (Navis et al, 2018). Regardless of the types of pain, in fact more than 50% of PLWH have moderate to severe pain that affects daily life (Miaskowski et al, 2011;Merlin et al, 2012).…”

Section: Epidemiologymentioning

confidence: 99%

Neuroinflammation in HIV-Related Neuropathic Pain

Wei

et al. 2021

Front. Pharmacol.

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In the management of human immunodeficiency virus (HIV) infection around the world, chronic complications are becoming a new problem along with the prolonged life expectancy. Chronic pain is widespread in HIV infected patients and even affects those with a low viral load undergoing long-term treatment with antiviral drugs, negatively influencing the adherence to disease management and quality of life. A large proportion of chronic pain is neuropathic pain, which defined as chronic pain caused by nervous system lesions or diseases, presenting a series of nervous system symptoms including both positive and negative signs. Injury caused by HIV protein, central and peripheral sensitization, and side effects of antiretroviral therapy lead to neuroinflammation, which is regarded as a maladaptive mechanism originally serving to promote regeneration and healing, constituting the main mechanism of HIV-related neuropathic pain. Gp120, as HIV envelope protein, has been found to be the major toxin that induces neuropathic pain. Particularly, the microglia, releasing numerous pro-inflammatory substances (such as TNFα, IL-1β, and IL-6), not only sensitize the neurons but also are the center part of the crosstalk bridging the astrocytes and oligodendrocytes together forming the central sensitization during HIV infection, which is not discussed detailly in recent reviews. In the meantime, some NRTIs and PIs exacerbate the neuroinflammation response. In this review, we highlight the importance of clarifying the mechanism of HIV-related neuropathic pain, and discuss about the limitation of the related studies as future research directions.

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“…In the western world, diabetes mellitus (DM) is the cause of polyneuropathy in around 30% to 40% of cases (2–5). Polyneuropathy can also be acquired secondary to a variety of other conditions including alcohol abuse, vitamin B 12 deficiency, human immunodeficiency virus (HIV) infection, chronic inflammatory demyelinating polyneuropathy (CIDP), and after chemotherapy (2,6,7). Furthermore, in 20% to 30% of the patients with polyneuropathy an underlying cause cannot be identified (1).…”

Section: Introductionmentioning

confidence: 99%