Evolving clinical phenotypes in HIV-associated neurocognitive disorders

Sacktor, Ned; Robertson, Kevin

doi:10.1097/coh.0000000000000102

Cited by 65 publications

(57 citation statements)

References 22 publications

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“…These results confirm what has been previously showed in cART experienced elderly HIV-infected subjects, where a mixed cortical-subcortical phenotype of impairment could be detected [9,41,42]. No cases of severe depression were found, thus reducing risks for confounding behavioural disorders.…”

Section: Discussionsupporting

confidence: 80%

Evaluation of Three Brief Screening Tests for Older Patients with Mild HIVAssociated Neurocognitive Disorders in the cART Era

Vassallo¹,

Barbaud²,

Fabre³

et al. 2017

J Neurol Neurophysiol

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Section: Discussionsupporting

confidence: 80%

Evaluation of Three Brief Screening Tests for Older Patients with Mild HIVAssociated Neurocognitive Disorders in the cART Era

Vassallo¹,

Barbaud²,

Fabre³

et al. 2017

J Neurol Neurophysiol

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“…Overall, contemporary combination antiretroviral therapy (ART) is highly successful in reducing CSF HIV RNA levels to below clinical detection limits in individuals with effective plasma virus suppression [7,8], and has also been highly effective in preventing the most severe complication of CNS HIV infection, HIVassociated dementia (HAD) related to HIV encephalitis [9,10].…”

Section: Introductionmentioning

confidence: 99%

Cerebrospinal Fluid HIV Escape from Antiretroviral Therapy

et al. 2015

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“…With the advent of highly active antiretroviral therapy (HAART), the severity of HAD has significantly decreased (34,52,53). However, subtler neurological disorders can arise even in individuals who are aviremic with HAART (54).…”

Section: Clinical Disorders Associated With Viral Replication In Macrmentioning

confidence: 99%

Macrophages in Progressive Human Immunodeficiency Virus/Simian Immunodeficiency Virus Infections

DiNapoli

Hirsch

Brenchley

2016

J Virol

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The cells that are targeted by primate lentiviruses (HIV and simian immunodeficiency virus [SIV]) are of intense interest given the renewed effort to identify potential cures for HIV. These viruses have been reported to infect multiple cell lineages of hematopoietic origin, including all phenotypic and functional CD4 T cell subsets. The two most commonly reported cell types that become infected in vivo are memory CD4 T cells and tissue-resident macrophages. Though viral infection of CD4 T cells is routinely detected in both HIV-infected humans and SIV-infected Asian macaques, significant viral infection of macrophages is only routinely observed in animal models wherein CD4 T cells are almost entirely depleted. Here we review the roles of macrophages in lentiviral disease progression, the evidence that macrophages support viral replication in vivo, the animal models where macrophage-mediated replication of SIV is thought to occur, how the virus can interact with macrophages in vivo, pathologies thought to be attributed to viral replication within macrophages, how viral replication in macrophages might contribute to the asymptomatic phase of HIV/SIV infection, and whether macrophages represent a long-lived reservoir for the virus. Macrophages are a diverse and functionally important component of the immune system. Evolutionarily conserved in almost all species of the phylum Chordata, macrophages are one of the "oldest" leukocyte lineages and have the highest degree of plasticity across leukocyte subsets (1). Macrophages differentiate from the yolk sac, fetal liver, and peripheral blood monocytes that developed from bone marrow-derived hematopoietic stem cells. With their phenotypic and functional plasticity and presence in disparate tissues, macrophages play supportive roles in multiple aspects of physiology. Their function often depends upon their anatomical location, their individual ontogeny, and extracellular cues. For example, macrophages derived from the yolk sac or fetal liver reside in organs such as the brain (as microglia cells), pancreas, spleen, liver (as Kuppfer cells), and kidney. For many years, yolk sac-and fetal liver-derived macrophages were thought to be very long-lived, perhaps for the life span of the host. Indeed, after differentiating during fetal development, these macrophages can populate tissues for the duration of the host's life. However, recent data suggest that these cells can also divide in vivo to maintain homeostasis (1-3) and are able to rapidly repopulate after chemotherapeutic depletion (in the case of brain-resident microglia cells [4]). Our understanding of macrophage longevity and factors important for their homeostatic proliferation in vivo is incomplete and more data are required. FUNCTIONS OF MACROPHAGES IN HEALTHThough macrophage longevity is not fully understood, many studies have demonstrated that tissue-resident macrophages have critically important functions in tissue immunity and repair, antigen presentation, and tissue homeostasis. Indeed, the importance of their fu...

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Evolving clinical phenotypes in HIV-associated neurocognitive disorders

Cited by 65 publications

References 22 publications

Evaluation of Three Brief Screening Tests for Older Patients with Mild HIVAssociated Neurocognitive Disorders in the cART Era

Evaluation of Three Brief Screening Tests for Older Patients with Mild HIVAssociated Neurocognitive Disorders in the cART Era

Cerebrospinal Fluid HIV Escape from Antiretroviral Therapy

Macrophages in Progressive Human Immunodeficiency Virus/Simian Immunodeficiency Virus Infections

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