Special Issue "HIV-Associated Neurocognitive Disorders (HAND)"

A special issue of Brain Sciences (ISSN 2076-3425).

Deadline for manuscript submissions: closed (28 February 2017).

Special Issue Editor

Dr. Jaime H. Vera Rojas
E-Mail Website
Guest Editor
Division of Infection and Global Health, Brighton and Sussex Medical School, Brighton, UK
Interests: HIV; cognitive impairment; HIV and aging
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Effective combination antiretroviral therapy (cART) has lead to a significant reduction in the prevalence and incidence of central nervous system (CNS) HIV-associated brain disease, particularly, CNS opportunistic infections and HIV encephalitis. Despite this, cognitive deficits in people living with HIV (PLWH) have become more apparent in recent years. The term HAND (HIV associated neurocognitive impairment) has been defined as cognitive impairment associated exclusively with HIV infection. However, defining if cognitive disorders in PLWH are due to HAND or other causes can be cumbersome on an individual basis. Several clinical risk factors that contribute towards cognitive impairment in PLWH, but are not specific to HIV infection per se, have been suggested, and include ageing, greater use of recreational drugs, increase rates of depression and anxiety, and high prevalence other comorbidities (cerebrovascular disease), and co-infections (hepatitis C and syphilis) that are known to affect the CNS. The development of HAND has been associated with antiretroviral therapy (poor drug concentration vs. neurotoxicity) and low-level CNS HIV replication, but more recently the role of brain immuneactivation in the development of HAND is taking central stage and could pave the wave for the development of new anti-inflammatory therapeutics for the management of HAND. As a result of a combination of successful viral control and enhanced survival with modern antiretroviral therapies, the global HIV-positive cohort is aging. There are concerns that an aging HIV population will be more prone to develop HAND, and therefore, novel strategies to treat and identify those individuals that are at most risk to develop HAND are urgently needed.

This Special Issue aims to describe factors associated with the development of HAND and other cognitive deficits affecting PLWH on effective cART, as well as describing novel strategies for the management of PLWH with cognitive difficulties.

Dr. Jaime Vera Rojas
Guest Editor

Manuscript Submission Information

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Keywords

  • HIV
  • HAND
  • cART

Published Papers (3 papers)

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Research

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Open AccessArticle
Hippocampal Neuronal Loss in Infant Macaques Orally Infected with Virulent Simian Immunodeficiency Virus (SIV)
Brain Sci. 2017, 7(4), 40; https://doi.org/10.3390/brainsci7040040 - 10 Apr 2017
Cited by 1
Abstract
The neurological impact of Human Immunodeficiency Virus (HIV) on children includes loss of brain growth, motor abnormalities and cognitive dysfunction. Despite early antiretroviral treatment (ART) intervention to suppress viral load, neurological consequences of perinatal HIV-1 infection persist. Utilizing the pediatric simian immunodeficiency virus [...] Read more.
The neurological impact of Human Immunodeficiency Virus (HIV) on children includes loss of brain growth, motor abnormalities and cognitive dysfunction. Despite early antiretroviral treatment (ART) intervention to suppress viral load, neurological consequences of perinatal HIV-1 infection persist. Utilizing the pediatric simian immunodeficiency virus (SIV) infection model, we tested the hypothesis that early-life SIV infection depletes neuronal population in the hippocampus. A total of 22 ART-naïve infant rhesus macaques (Macaca mulatta) from previous studies were retrospectively analyzed. Infant macaques were either intravenously (IV) inoculated with highly virulent SIVmac251 at ~1 week of age and monitored for 6–10 weeks, or orally challenged with SIVmac251 from week 9 of age onwards with a monitoring period of 10–23 weeks post-infection (19–34 weeks of age), and SIV-uninfected controls were euthanized at 16–17 weeks of age. We have previously reported that the IV SIVmac251-infected neonatal macaques (Group 1) displayed a 42% neuronal reduction throughout the hippocampal cornu ammonis (CA) fields. The orally-infected infant macaques displayed a 75% neuronal reduction in the CA1 region compared to controls and 54% fewer neurons than IV SIV infants. The CA2 region showed a similar pattern, with a 67% reduction between orally-infected SIV subjects and controls and a 40% difference between IV-and orally-infected SIV groups. In the CA3 region, there were no significant differences between these groups, however both SIV-infected groups had significantly fewer pyramidal neurons than control subjects. There was no correlation between plasma viral load and neuronal populations in any of the CA fields. The loss of hippocampal neurons may contribute to the rapid neurocognitive decline associated with pediatric HIV infection. While each subfield showed vulnerability to SIV infection, the CA1 and CA2 subregions demonstrated a potentially enhanced vulnerability to pediatric SIV infection. These data underscore the need for early diagnosis and treatment, including therapeutics targeting the central nervous system (CNS). Full article
(This article belongs to the Special Issue HIV-Associated Neurocognitive Disorders (HAND))
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Review

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Open AccessReview
The Role of HIV Infection in Neurologic Injury
Brain Sci. 2017, 7(4), 38; https://doi.org/10.3390/brainsci7040038 - 06 Apr 2017
Cited by 10
Abstract
The central nervous system (CNS) is a very challenging HIV-1 sanctuary, in which HIV-1 replication is established early on during acute infection and can persist despite potent antiretroviral treatments. HIV-1 infected macrophages play a pivotal role acting as vehicles for HIV-1 to spread [...] Read more.
The central nervous system (CNS) is a very challenging HIV-1 sanctuary, in which HIV-1 replication is established early on during acute infection and can persist despite potent antiretroviral treatments. HIV-1 infected macrophages play a pivotal role acting as vehicles for HIV-1 to spread into the brain, and can be the major contributor of an early compartmentalization. HIV-1 infection in CNS may lead to a broad spectrum of neurological syndromes, such as dementia, mild neurocognitive disorders, and asymptomatic impairment. These clinical manifestations are caused by the release of neurotoxins from infected cells (mainly macrophages), and also by several HIV-1 proteins, able to activate cell-signaling involved in the control of cellular survival and apoptosis. This review is aimed at highlighting the virological aspects associated with the onset of neurocognitive disorders and at addressing the novel therapeutic approaches to stop HIV-1 replication in this critical sanctuary. Full article
(This article belongs to the Special Issue HIV-Associated Neurocognitive Disorders (HAND))
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Open AccessFeature PaperReview
Neuronal Stress and Injury Caused by HIV-1, cART and Drug Abuse: Converging Contributions to HAND
Brain Sci. 2017, 7(3), 25; https://doi.org/10.3390/brainsci7030025 - 23 Feb 2017
Cited by 9
Abstract
Multiple mechanisms appear to contribute to neuronal stress and injury underlying HIV-associated neurocognitive disorders (HAND), which occur despite the successful introduction of combination antiretroviral therapy (cART). Evidence is accumulating that components of cART can itself be neurotoxic upon long-term exposure. In addition, abuse [...] Read more.
Multiple mechanisms appear to contribute to neuronal stress and injury underlying HIV-associated neurocognitive disorders (HAND), which occur despite the successful introduction of combination antiretroviral therapy (cART). Evidence is accumulating that components of cART can itself be neurotoxic upon long-term exposure. In addition, abuse of psychostimulants, such as methamphetamine (METH), seems to compromise antiretroviral therapy and aggravate HAND. However, the combined effect of virus and recreational and therapeutic drugs on the brain is still incompletely understood. However, several lines of evidence suggest a shared critical role of oxidative stress, compromised neuronal energy homeostasis and autophagy in promotion and prevention of neuronal dysfunction associated with HIV-1 infection, cART and psychostimulant use. In this review, we present a synopsis of recent work related to neuronal stress and injury induced by HIV infection, antiretrovirals (ARVs) and the highly addictive psychostimulant METH. Full article
(This article belongs to the Special Issue HIV-Associated Neurocognitive Disorders (HAND))
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