74 Citations (Scopus)

Abstract

HIV enters the brain soon after virus exposure but elicits profound neurological deficits in infected humans years later usually during progressive immunosuppression and the development of the acquired immune deficiency syndrome. The neurological disease complex associated with virus infection occurs in a large proportion of infected patients and is commonly referred to as HIV-1 associated dementia complex. The neuropathogenesis of central nervous system/viral infection revolves around mononuclear phagocytes (brain macrophage/microglial) infection and immune activation in brain. Macrophages secrete neurotoxic factors that elicit neuronal injury and inevitably death leading to the constellation of cognitive and motor impairments common during progressive disease. Neurotoxic factor production requires virus entry and replication, the evolution/selection of neurovirulent HIV-1 strains and the production of viral and cellular immune factors injurious to human neurons. Interestingly, neurological deficits, the HIV-1 associated neuropathology and viral replication disease are not always associated. This has led to the notion that viral replication induces the autocrine/paracrine production of cellular/viral factors leading to a metabolic encephalopathy. Anti-retroviral and anti-inflammatory therapies should prove increasingly beneficial for treatment and, ultimately, reversal of HIV-1 associated dementia complex in the affected human host.

Original languageEnglish (US)
Pages (from-to)319-325
Number of pages7
JournalCurrent Opinion in Neurology
Volume10
Issue number4
StatePublished - Sep 4 1997

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Metabolic Brain Diseases
Phagocytes
Dementia
HIV-1
Virus Diseases
Brain
Central Nervous System Viral Diseases
Macrophages
Satellite Viruses
Virus Internalization
Immunologic Factors
Virus Replication
Immunosuppression
Acquired Immunodeficiency Syndrome
Anti-Inflammatory Agents
HIV
Viruses
Neurons
Wounds and Injuries
Therapeutics

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this

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title = "The HIV-1 associated dementia complex: A metabolic encephalopathy fueled by viral replication in mononuclear phagocytes",
abstract = "HIV enters the brain soon after virus exposure but elicits profound neurological deficits in infected humans years later usually during progressive immunosuppression and the development of the acquired immune deficiency syndrome. The neurological disease complex associated with virus infection occurs in a large proportion of infected patients and is commonly referred to as HIV-1 associated dementia complex. The neuropathogenesis of central nervous system/viral infection revolves around mononuclear phagocytes (brain macrophage/microglial) infection and immune activation in brain. Macrophages secrete neurotoxic factors that elicit neuronal injury and inevitably death leading to the constellation of cognitive and motor impairments common during progressive disease. Neurotoxic factor production requires virus entry and replication, the evolution/selection of neurovirulent HIV-1 strains and the production of viral and cellular immune factors injurious to human neurons. Interestingly, neurological deficits, the HIV-1 associated neuropathology and viral replication disease are not always associated. This has led to the notion that viral replication induces the autocrine/paracrine production of cellular/viral factors leading to a metabolic encephalopathy. Anti-retroviral and anti-inflammatory therapies should prove increasingly beneficial for treatment and, ultimately, reversal of HIV-1 associated dementia complex in the affected human host.",
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T1 - The HIV-1 associated dementia complex

T2 - A metabolic encephalopathy fueled by viral replication in mononuclear phagocytes

AU - Zheng, Jialin C

AU - Gendelman, Howard Eliot

PY - 1997/9/4

Y1 - 1997/9/4

N2 - HIV enters the brain soon after virus exposure but elicits profound neurological deficits in infected humans years later usually during progressive immunosuppression and the development of the acquired immune deficiency syndrome. The neurological disease complex associated with virus infection occurs in a large proportion of infected patients and is commonly referred to as HIV-1 associated dementia complex. The neuropathogenesis of central nervous system/viral infection revolves around mononuclear phagocytes (brain macrophage/microglial) infection and immune activation in brain. Macrophages secrete neurotoxic factors that elicit neuronal injury and inevitably death leading to the constellation of cognitive and motor impairments common during progressive disease. Neurotoxic factor production requires virus entry and replication, the evolution/selection of neurovirulent HIV-1 strains and the production of viral and cellular immune factors injurious to human neurons. Interestingly, neurological deficits, the HIV-1 associated neuropathology and viral replication disease are not always associated. This has led to the notion that viral replication induces the autocrine/paracrine production of cellular/viral factors leading to a metabolic encephalopathy. Anti-retroviral and anti-inflammatory therapies should prove increasingly beneficial for treatment and, ultimately, reversal of HIV-1 associated dementia complex in the affected human host.

AB - HIV enters the brain soon after virus exposure but elicits profound neurological deficits in infected humans years later usually during progressive immunosuppression and the development of the acquired immune deficiency syndrome. The neurological disease complex associated with virus infection occurs in a large proportion of infected patients and is commonly referred to as HIV-1 associated dementia complex. The neuropathogenesis of central nervous system/viral infection revolves around mononuclear phagocytes (brain macrophage/microglial) infection and immune activation in brain. Macrophages secrete neurotoxic factors that elicit neuronal injury and inevitably death leading to the constellation of cognitive and motor impairments common during progressive disease. Neurotoxic factor production requires virus entry and replication, the evolution/selection of neurovirulent HIV-1 strains and the production of viral and cellular immune factors injurious to human neurons. Interestingly, neurological deficits, the HIV-1 associated neuropathology and viral replication disease are not always associated. This has led to the notion that viral replication induces the autocrine/paracrine production of cellular/viral factors leading to a metabolic encephalopathy. Anti-retroviral and anti-inflammatory therapies should prove increasingly beneficial for treatment and, ultimately, reversal of HIV-1 associated dementia complex in the affected human host.

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M3 - Review article

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JO - Current Opinion in Neurology

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