Preventing Brain Damage In HIV Infection
Preventing Brain Damage In HIV Infection
HIV-1 is a virus with neurotropic features causing major morbidity and also mortality if untreated. Mild symptoms of neurocognitive impairment are common and precede more severe forms of dementia, termed AIDS dementia complex (ADC). The pathogenesis of neurodegeneration in HIV-1 infection is not fully understood, and we lack specific markers to verify the diagnosis. Fortunately, antiretroviral treatment is effective in treating both systemic and CNS infection, and neurocognitive symptoms and ADC will, in most cases, improve on treatment. This review focuses on current research regarding cerebral spinal fluid biomarkers and effects of highly active antiretroviral treatment on HIV-1 CNS disease.
HIV-1 (hereafter referred to as HIV) is a neurotropic virus, affecting both the peripheral nervous system and CNS. HIV has been isolated from the cerebrospinal fluid (CSF), brain tissue, spinal cord and sural nerve in neurologically symptomatic patients. HIV enters the CNS very soon after infection, at the time of primary infection or seroconversion, and HIV RNA can be detected in CSF in the majority of patients, irrespective of stage. The common view of how HIV enters the CNS is by infiltration of infected monocytes across the BBB, the 'Trojan horse' mechanism, as further described by Albright et al. in 2003. Other proposed routes are release of the virus from infected brain microvascular endothelial cells or a direct passage of cell-free virus through the BBB, reviewed in detail by Kramer-Hämmerle et al. Infected monocytes then differentiate into macrophages, replenishing resident brain macrophages and also producing virions that can infect other cells, astrocytes and microglia - the resident macrophages in the brain.
HIV-1 is a virus with neurotropic features causing major morbidity and also mortality if untreated. Mild symptoms of neurocognitive impairment are common and precede more severe forms of dementia, termed AIDS dementia complex (ADC). The pathogenesis of neurodegeneration in HIV-1 infection is not fully understood, and we lack specific markers to verify the diagnosis. Fortunately, antiretroviral treatment is effective in treating both systemic and CNS infection, and neurocognitive symptoms and ADC will, in most cases, improve on treatment. This review focuses on current research regarding cerebral spinal fluid biomarkers and effects of highly active antiretroviral treatment on HIV-1 CNS disease.
HIV-1 (hereafter referred to as HIV) is a neurotropic virus, affecting both the peripheral nervous system and CNS. HIV has been isolated from the cerebrospinal fluid (CSF), brain tissue, spinal cord and sural nerve in neurologically symptomatic patients. HIV enters the CNS very soon after infection, at the time of primary infection or seroconversion, and HIV RNA can be detected in CSF in the majority of patients, irrespective of stage. The common view of how HIV enters the CNS is by infiltration of infected monocytes across the BBB, the 'Trojan horse' mechanism, as further described by Albright et al. in 2003. Other proposed routes are release of the virus from infected brain microvascular endothelial cells or a direct passage of cell-free virus through the BBB, reviewed in detail by Kramer-Hämmerle et al. Infected monocytes then differentiate into macrophages, replenishing resident brain macrophages and also producing virions that can infect other cells, astrocytes and microglia - the resident macrophages in the brain.
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