Peripheral immune dysregulation in the ART era of HIV-associated neurocognitive impairments: A systematic review

Williams, Monray E.; Ipser, Jonathan; Stein, Dan J.; Joska, John A.; Naudé, Petrus J.W.

doi:10.1016/j.psyneuen.2020.104689

Cited by 21 publications

(21 citation statements)

References 68 publications

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“…Should COVID-19 contribute to (neuro)inflammation, what may this mean for patients with HAND who already experience dysregulated (neuro)inflammatory levels? 7,9,10,30,143 Preliminary evidence suggests that COVID-19 may exacerbate systemic and neuroinflammation, with common findings reported for IL-6. IL-6 is a predominant component of CSS and the pathway of IL-6 dysregulation may be important in the pathophysiology of COVID-19.…”

Section: Potential Contributions Of Covid-19 To (Neuro)inflammation In Plwhmentioning

confidence: 83%

“…6 Regardless of viral suppression and CD4 count, HIV-positive participants report dysregulated inflammatory levels and the dysregulated levels are associated with HAND. [7][8][9][10][11] Therefore, low-grade neuroinflammation may be a key pathway in the development of HAND. What are the implications for the development of HAND if another virus were to enter the CNS, eliciting a major immune response such as a cytokine storm and exacerbating the current low-grade inflammation in PLWH?…”

Section: Introductionmentioning

confidence: 99%

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Insult to Injury-Potential Contribution of Coronavirus Disease-19 to Neuroinflammation and the Development of HIV-Associated Neurocognitive Disorders

Williams

Fielding

2021

AIDS Research and Human Retroviruses

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Severe acute respiratory syndrome (SARS)-coronavirus (CoV)-2 is responsible for a new coronavirus disease known as coronavirus disease-19 (COVID-19). SARS-CoV-2 reports neurotropic properties and may have neurological implications, and this creates another health burden for people living with HIV. As yet, the impact of COVID-19 on (neuro)inflammation and the development of HIV-associated neurocognitive disorders (HAND) is not fully known. Here, we reviewed preliminary evidence that provides clues that COVID-19 may exacerbate inflammatory mechanisms related to the development of HAND.

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Section: Potential Contributions Of Covid-19 To (Neuro)inflammation In Plwhmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Insult to Injury-Potential Contribution of Coronavirus Disease-19 to Neuroinflammation and the Development of HIV-Associated Neurocognitive Disorders

Williams

Fielding

2021

AIDS Research and Human Retroviruses

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“…Myo-inositol is a marker of glial activation and inflammation and is associated with the level of inflammation (C-reactive protein) (Haroon et al, 2016). Cerebral myo-inositol (Young et al, 2014) and peripheral inflammatory (Williams et al, 2020) levels were reported to be persistently elevated in HIV-positive participants regardless of treatment 1, and a tyrosine 3/tryptophan 5-monooxygenase activation protein.…”

Section: Discussionmentioning

confidence: 99%

“…Myo‐inositol is a marker of glial activation and inflammation and is associated with the level of inflammation (C‐reactive protein) (Haroon et al., 2016). Cerebral myo‐inositol (Young et al., 2014) and peripheral inflammatory (Williams et al., 2020) levels were reported to be persistently elevated in HIV‐positive participants regardless of treatment status. Myo‐inositol levels were associated with neurocognitive dysfunction in patients with Alzheimer's disease (Voevodskaya et al., 2016) and mild cognitive impairment (Huang et al., 1999).…”

Section: Discussionmentioning

confidence: 99%

“…Within the CNS, HIV can act via several direct and indirect mechanism which results in neuronal apoptosis (András et al., 2003; González‐Scarano & Martín‐García, 2005; Kaul & Lipton, 1999; Meucci et al., 1998; Patel et al., 2002). In participants with HAND, several neurobiological mechanisms may be active and these may be recorded as irregular levels of proteins, metabolites (Cotto et al., 2019), and inflammatory cytokines/chemokines (Williams et al., 2020). Despite many promising reports, there are no markers with the potential for predicting or stratifying the risk of neurocognitive impairment in people living with HIV (PLWH).…”

Section: Introductionmentioning

confidence: 99%

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Proteomics and metabolomics of HIV‐associated neurocognitive disorders: A systematic review

Williams

Naudé

Westhuizen

2021

Journal of Neurochemistry

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HIV-associated neurocognitive disorders (HAND) are common features of the effect of human immunodeficiency virus (HIV)-1 within the central nervous system (CNS).The underlying neuropathophysiology of HAND is incompletely known. Furthermore, there are no markers to effectively predict or stratify the risk of HAND. Recent advancements in the fields of proteomics and metabolomics have shown promise in addressing these concerns, however, it is not clear if these approaches may provide new insight into pathways and markers related to HAND. We therefore conducted a

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HIV and inflammatory markers are associated with persistent COVID‐19 symptoms

Kamanzi,

Mulundu,

Mutale

et al. 2023

Immunity Inflam & Disease

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Background A proportion of COVID19 survivors may present with long‐COVID, which is persistent symptoms lasting four or more weeks post SARS‐CoV‐2 infection. These symptoms may be mild to severe, and may affect different organ‐systems of the body. Aims The main objective of this study was to determine the demographic, clinical and immunological factors associated with long COVID. Materials & Methods We conducted a nested case control study, with a total of 94 study participants initially included, and 64 participants matched for age and sex for biomarker analyses. Results 32/94 (34.1%) of all the participants had long COVID. Respiratory symptoms were the most common (59.5%) followed by the musculoskeletal symptoms (28.1%). HIV was an independent predictor of long COVID (adjusted odds ratio = 2.7; p = .037). In all the 64 matched cases and controls, IFN‐β was significantly higher among controls than cases. After stratifying by HIV, IL6 was significantly higher among cases than controls in the HIV‐ group (2.06 vs. 0.81 pg/mL; p = .02). On the other hand, IFN‐β was significantly higher among controls than cases in the HIV+ group (251 vs. 0 pg/mL; p = .01). Conclusion HIV infection is a risk factor for long COVID, and inflammatory markers associated with long COVID may be slightly different for HIV− and HIV+ individuals.

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Peripheral immune dysregulation in the ART era of HIV-associated neurocognitive impairments: A systematic review

Cited by 21 publications

References 68 publications

Insult to Injury-Potential Contribution of Coronavirus Disease-19 to Neuroinflammation and the Development of HIV-Associated Neurocognitive Disorders

Insult to Injury-Potential Contribution of Coronavirus Disease-19 to Neuroinflammation and the Development of HIV-Associated Neurocognitive Disorders

Proteomics and metabolomics of HIV‐associated neurocognitive disorders: A systematic review

HIV and inflammatory markers are associated with persistent COVID‐19 symptoms

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