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Find video protocols related to scientific articles indexed in Pubmed.
Cerebral metabolite changes prior to and after antiretroviral therapy in primary HIV infection.
Neurology
PUBLISHED: 09-26-2014
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We examined the longitudinal effects of primary HIV infection (PHI) and responses to early antiretroviral therapy (ART) on the brain using high-field magnetic resonance spectroscopy (MRS).
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Treatment of HIV in the CNS: effects of antiretroviral therapy and the promise of non-antiretroviral therapeutics.
Curr HIV/AIDS Rep
PUBLISHED: 07-27-2014
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The growing recognition of the burden of neurologic disease associated with HIV infection in the last decade has led to renewed efforts to characterize the pathophysiology of the virus within the central nervous system (CNS). The concept of the AIDS-dementia complex is now better understood as a spectrum of HIV-associated neurocognitive disorders (HAND), which range from asymptomatic disease to severe impairment. Recent work has shown that even optimally treated patients can experience not only persistent HAND, but also the development of new neurologic abnormalities despite viral suppression. This has thrown into question what the impact of antiretroviral therapy has been on the incidence and prevalence of neurocognitive dysfunction. In this context, the last few years have seen a concentrated effort to identify the effects that antiretroviral therapy has on the neurologic manifestations of HIV and to develop therapeutic modalities that might specifically alter the trajectory of HIV within the CNS.
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CROI 2014: neurologic complications of HIV infection.
Top Antivir Med
PUBLISHED: 06-06-2014
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A shift in focus in the field of neuroHIV was clearly manifest at the 2014 Conference on Retroviruses and Opportunistic Infections (CROI), where a major emphasis was on the milder forms of neurologic morbidity, including cognitive impairment, seen in well-treated patients. Mechanisms of this persistent abnormality were investigated, including extensive analysis of the prevalence and associations of persistent HIV detection in cerebrospinal fluid (CSF) and characterization of persistent CNS immune activation. Another key emphasis was the early establishment of HIV replication and inflammation within the central nervous system (CNS) and the potentially salutary effect of very early HIV diagnosis and treatment in protecting the CNS from HIV-related injury. Mitochondrial function was identified as a potential mediator of a number of aspects of HIV-associated CNS dysfunction, including neurotoxicity associated with efavirenz, host genetic determinants of HIV-associated neurocognitive disorders (HAND), associations with direct measures of mitochondria in CSF, and metabolomic screening of CSF in HIV-infected subjects and those with HAND. Many studies employed laboratory rather than neuropsychologic end points, with a major focus on CSF biomarkers. Overall, neuroHIV presentations at CROI 2014 provided new insights into pathogenesis and treatment of the CNS, raising new challenges for researchers and practitioners aiming to optimize the status of the brain in people living with HIV infection.
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Peripheral neuropathy in primary HIV infection associates with systemic and central nervous system immune activation.
J. Acquir. Immune Defic. Syndr.
PUBLISHED: 04-16-2014
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Peripheral neuropathy (PN) is a frequent complication of chronic HIV infection. We prospectively studied individuals with primary HIV infection (<1 year after transmission) to assess the presence of and laboratory associations with PN in this early stage.
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Evolving character of chronic central nervous system HIV infection.
Semin Neurol
PUBLISHED: 04-08-2014
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Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system (CNS) begins early in systemic infection and continues throughout its untreated course. Despite a common cerebrospinal fluid inflammatory response, it is usually neurologically asymptomatic for much of this course, but can evolve in some individuals to HIV-associated dementia (HAD), a severe encephalopathy with characteristic cognitive and motor dysfunction. While widespread use of combination antiretroviral therapy (ART) has led to a marked decline in both the CNS infection and its neurologic severe consequence, HAD continues to afflict individuals presenting with advanced systemic infection in the developed world and a larger number in resource-poor settings where ART is more restricted. Additionally, milder CNS injury and dysfunction have broader prevalence, including in those treated with ART. Here we review the history and evolving nomenclature of HAD, its viral pathogenesis, clinical presentation and diagnosis, and treatment.
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Longitudinal characterization of depression and mood states beginning in primary HIV infection.
AIDS Behav
PUBLISHED: 01-04-2014
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Though depression is known to frequently afflict those with chronic HIV, mood during the early course of HIV is not well characterized. In a prospective study we assessed mood during primary HIV infection [primary HIV infection (PHI), <1 year duration], its association with neuropsychological performance and markers of neurological disease, and its longitudinal course including effects of antiretroviral therapy (ART). The Beck Depression Inventory (BDI) and Profile of Mood States (POMS) subscales were longitudinally administered prior to and after ART in PHI subjects. This evaluation of mood was done concurrently with blood, cerebrospinal fluid (CSF) and neuropsychological [total z and global deficit score (GDS)] evaluation at each visit. Analysis employed Spearman's rho, logistic regression, and linear mixed models. 47.7 % of the 65 men recruited at a median 3.5 months HIV duration met BDI criteria for clinical depression at baseline, classified as 'mild' (n = 11), 'moderate' (n = 11), or 'severe' (n = 9). Drug, alcohol, and depression history did not associate with BDI score. Proportional somatic-performance scores were worse than cognitive-affective scores (p = .0045). Vigor subscore of POMS was reduced compared to norms and correlated with total z (r = 0.33, p = 0.013) and GDS (r = -0.32, p = 0.016). BDI and POMS correlated with one another (r = 0.85, p < .0001), but not with CSF or plasma HIV RNA, WBC, albumin ratio or neopterin. Improvement was not observed in BDI and POMS over 330 total follow-up visits, even after initiation of ART. Depression was prevalent during PHI in our subjects, associated with abnormal somatic-performance and vigor scores. Neither neuropsychological performance nor disease biomarkers correlated with depressed mood. Mood indices did not improve over time in the presence of ART.
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An example of genetically distinct HIV-1 variants in cerebrospinal fluid and plasma during suppressive therapy.
J. Infect. Dis.
PUBLISHED: 12-12-2013
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We sequenced HIV-1 in 70 CSF and 29 plasma samples and the corresponding pre-therapy samples from 17 subjects on suppressive therapy. More of the CSF sequences were hypermutants than plasma sequences. We generated on-therapy sequences from both CSF and plasma from two subjects; in one we found genetically distinct sequences in CSF and plasma indicating that they came from two different compartments, one potentially the CNS, during suppressive therapy. In addition, there was little evidence of viral evolution in the CSF during therapy, suggesting that continuous virus replication is not the major cause of viral persistence in the CNS.
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Single-copy assay quantification of HIV-1 RNA in paired cerebrospinal fluid and plasma samples from elite controllers.
AIDS
PUBLISHED: 11-13-2013
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Elite controllers are a rare subset of HIV-1-infected individuals who maintain HIV-1 RNA concentrations in plasma below the lower limit of quantification of clinical assays (<20-50 copies/ml) in the absence of antiretroviral therapy. Here, we examine to what extent elite controllers also control infection of the central nervous system (CNS).
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Neurologic complications of HIV infection: highlights from the 2013 Conference on Retroviruses and Opportunistic Infections.
Top Antivir Med
PUBLISHED: 08-29-2013
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Thirty years into the HIV epidemic, the management and investigation of neurologic complications of HIV disease have evolved from a struggle to understand and treat inexorable disorders to an optimistic effort to address more subtle but often complex conditions in patients surviving long-term with a chronic disease. Although severe forms of HIV encephalitis and HIV-associated dementia, myelopathy, opportunistic infections, and neuropathy are still frequently encountered entities where access to HIV treatment is limited, in settings with sufficient resources, they are predominantly seen in those who present late to care or are unable to maintain consistent antiretroviral adherence. In 2013, practitioners, patients, and investigators can realistically aim for an outstanding quality of life for those living with HIV infection and seek to reduce morbidity associated with milder forms of HIV-associated neurocognitive disorder (HAND). Neurologic presentations at the 20th Conference on Retroviruses and Opportunistic Infections (CROI) reflected this now well-established paradigm shift, focusing on treatment strategies to optimize neurologic and cognitive function, the pathogenesis of HAND in the current era, imaging biomarkers of HAND, the confluence of HIV infection and aging, and characterization of central nervous system HIV reservoirs of infection.
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HIV and neurocognitive dysfunction.
Curr HIV/AIDS Rep
PUBLISHED: 07-18-2013
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The spectrum of HIV-associated neurocognitive disorder (HAND) has been dramatically altered in the setting of widely available effective antiretroviral therapy (ART). Once culminating in dementia in many individuals infected with HIV, HAND now typically manifests as more subtle, though still morbid, forms of cognitive impairment in persons surviving long-term with treated HIV infection. Despite the substantial improvement in severity of this disorder, the fact that neurologic injury persists despite ART remains a challenge to the community of patients, providers and investigators aiming to optimize quality of life for those living with HIV. Cognitive dysfunction in treated HIV may reflect early irreversible CNS injury accrued before ART is typically initiated, ongoing low-level CNS infection and progressive injury in the setting of ART, or comborbidities including effects of treatment which may confound the beneficial reduction in viral replication and immune activation effected by ART.
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Approach to Cerebrospinal Fluid (CSF) Biomarker Discovery and Evaluation in HIV Infection.
J Neuroimmune Pharmacol
PUBLISHED: 05-28-2013
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Central nervous system (CNS) infection is a nearly universal facet of systemic HIV infection that varies in character and neurological consequences. While clinical staging and neuropsychological test performance have been helpful in evaluating patients, cerebrospinal fluid (CSF) biomarkers present a valuable and objective approach to more accurate diagnosis, assessment of treatment effects and understanding of evolving pathobiology. We review some lessons from our recent experience with CSF biomarker studies. We have used two approaches to biomarker analysis: targeted, hypothesis-driven and non-targeted exploratory discovery methods. We illustrate the first with data from a cross-sectional study of defined subject groups across the spectrum of systemic and CNS disease progression and the second with a longitudinal study of the CSF proteome in subjects initiating antiretroviral treatment. Both approaches can be useful and, indeed, complementary. The first is helpful in assessing known or hypothesized biomarkers while the second can identify novel biomarkers and point to broad interactions in pathogenesis. Common to both is the need for well-defined samples and subjects that span a spectrum of biological activity and biomarker concentrations. Previously-defined guide biomarkers of CNS infection, inflammation and neural injury are useful in categorizing samples for analysis and providing critical biological context for biomarker discovery studies. CSF biomarkers represent an underutilized but valuable approach to understanding the interactions of HIV and the CNS and to more objective diagnosis and assessment of disease activity. Both hypothesis-based and discovery methods can be useful in advancing the definition and use of these biomarkers.
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Cerebrospinal fluid and neuroimaging biomarker abnormalities suggest early neurological injury in a subset of individuals during primary HIV infection.
J. Infect. Dis.
PUBLISHED: 03-04-2013
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Cerebrospinal fluid (CSF) and neuroimaging abnormalities demonstrate neuronal injury during chronic AIDS, but data on these biomarkers during primary human immunodeficiency virus (HIV) infection is limited.
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Cerebrospinal fluid neopterin decay characteristics after initiation of antiretroviral therapy.
J Neuroinflammation
PUBLISHED: 02-04-2013
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Neopterin, a biomarker of macrophage activation, is elevated in the cerebrospinal fluid (CSF) of most HIV-infected individuals and decreases after initiation of antiretroviral therapy (ART). We studied decay characteristics of neopterin in CSF and blood after commencement of ART in HIV-infected subjects and estimated the set-point levels of CSF neopterin after ART-mediated viral suppression.
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Cellular Composition of Cerebrospinal Fluid in HIV-1 Infected and Uninfected Subjects.
PLoS ONE
PUBLISHED: 01-01-2013
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In order to characterize the cellular composition of cerebrospinal fluid (CSF) in a healthy state and in the setting of chronic pleocytosis associated with HIV-1 (HIV) infection, multi-parameter flow cytometry was used to identify and quantitate cellular phenotypes in CSF derived from HIV-uninfected healthy controls and HIV-infected subjects across a spectrum of disease and treatment. CD4+ T cells were the most frequent CSF population and the CD4:CD8 ratio was significantly increased in the CSF compared to blood (p?=?0.0232), suggesting preferential trafficking of CD4+ over CD8+ T cells to this compartment. In contrast, in HIV-infection, CD8+ T cells were the major cellular component of the CSF and were markedly increased compared to HIV-uninfected subjects (p<0.001). As with peripheral blood, the CSF CD4:CD8 ratio was reversed in HIV-infected subjects compared to HIV-uninfected subjects. Monocytes, B cells and NK cells were rare in the CSF in both groups, although absolute counts of CSF NK cells and B cells were significantly increased in HIV-infected subjects (p<0.05). Our studies show that T cells are the major cellular component of the CSF in HIV-infected and uninfected subjects. The CSF pleocytosis characteristic of HIV infection involves all lymphocyte subsets we measured, except for CD4+ T cells, but is comprised primarily of CD8+ T cells. The reduced proportion of CD4+ T cells in the CSF may reflect both HIV-related peripheral loss and changes in trafficking patterns in response to HIV infection in the central nervous system.
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Raltegravir treatment intensification does not alter cerebrospinal fluid HIV-1 infection or immunoactivation in subjects on suppressive therapy.
J. Infect. Dis.
PUBLISHED: 10-21-2011
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Despite suppression of plasma human immunodeficiency virus type 1 (HIV-1) RNA by antiretroviral therapy to levels below clinical assay detection, infection and immune activation may persist within the central nervous system and possibly lead to continued brain injury. We hypothesized that intensifying therapy would decrease cerebrospinal fluid (CSF) infection and immune activation.
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Central nervous system complications of HIV infection.
Top Antivir Med
PUBLISHED: 08-27-2011
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Issues relevant to the nervous system garnered substantial attention at the 18th Conference on Retroviruses and Opportunistic Infections. Several topics emerged as areas of importance both for informing current understanding of HIV-related neurologic disorders and their treatment, and for spurring future investigations. Measurable biomarkers of HIV-associated neurocognitive disorder (HAND) were a major theme, with studies ranging from new investigations of known laboratory and imaging markers to identification of novel molecules that might be investigated as potential means to follow disease activity as well as to better understand etiology of disease. Studies of pathogenesis of HAND and simian immunodeficiency virus-mediated neurologic injury added to prior understanding of lentivirus neuropathogenesis. Another broad area of investigation was the interplay between treatment with antiretroviral or adjunctive therapies and biomarkers of HAND. New data were presented on the potential importance of acute and early infection on the integrity of the central nervous system, complemented by studies of the effects of early treatment interventions.
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Central nervous system immune activation characterizes primary human immunodeficiency virus 1 infection even in participants with minimal cerebrospinal fluid viral burden.
J. Infect. Dis.
PUBLISHED: 08-17-2011
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Central nervous system (CNS) human immunodeficiency virus (HIV) infection and immune activation lead to brain injury and neurological impairment. Although HIV enters the nervous system soon after transmission, the magnitude of infection and immunoactivation within the CNS during primary HIV infection (PHI) has not been characterized.
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HIV-1 replication in the central nervous system occurs in two distinct cell types.
PLoS Pathog.
PUBLISHED: 06-18-2011
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Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system (CNS) can lead to the development of HIV-1-associated dementia (HAD). We examined the virological characteristics of HIV-1 in the cerebrospinal fluid (CSF) of HAD subjects to explore the association between independent viral replication in the CNS and the development of overt dementia. We found that genetically compartmentalized CCR5-tropic (R5) T cell-tropic and macrophage-tropic HIV-1 populations were independently detected in the CSF of subjects diagnosed with HIV-1-associated dementia. Macrophage-tropic HIV-1 populations were genetically diverse, representing established CNS infections, while R5 T cell-tropic HIV-1 populations were clonally amplified and associated with pleocytosis. R5 T cell-tropic viruses required high levels of surface CD4 to enter cells, and their presence was correlated with rapid decay of virus in the CSF with therapy initiation (similar to virus in the blood that is replicating in activated T cells). Macrophage-tropic viruses could enter cells with low levels of CD4, and their presence was correlated with slow decay of virus in the CSF, demonstrating a separate long-lived cell as the source of the virus. These studies demonstrate two distinct virological states inferred from the CSF virus in subjects diagnosed with HAD. Finally, macrophage-tropic viruses were largely restricted to the CNS/CSF compartment and not the blood, and in one case we were able to identify the macrophage-tropic lineage as a minor variant nearly two years before its expansion in the CNS. These results suggest that HIV-1 variants in CSF can provide information about viral replication and evolution in the CNS, events that are likely to play an important role in HIV-associated neurocognitive disorders.
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Minocycline fails to modulate cerebrospinal fluid HIV infection or immune activation in chronic untreated HIV-1 infection: results of a pilot study.
AIDS Res Ther
PUBLISHED: 01-14-2011
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Minocycline is a tetracycline antibiotic that has been shown to attenuate central nervous system (CNS) lentivirus infection, immune activation, and brain injury in model systems. To initiate assessment of minocycline as an adjuvant therapy in human CNS HIV infection, we conducted an open-labelled pilot study of its effects on cerebrospinal fluid (CSF) and blood biomarkers of infection and immune responses in 7 viremic subjects not taking antiretroviral therapy.
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HIV-1 viral escape in cerebrospinal fluid of subjects on suppressive antiretroviral treatment.
J. Infect. Dis.
PUBLISHED: 11-04-2010
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Occasional cases of viral escape in cerebrospinal fluid (CSF) despite suppression of plasma human immunodeficiency virus type 1 (HIV-1) RNA have been reported. We investigated CSF viral escape in subjects treated with commonly used antiretroviral therapy regimens in relation to intrathecal immune activation and central nervous system penetration effectiveness (CPE) rank.
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Cerebrospinal fluid in HIV-1 systemic viral controllers: absence of HIV-1 RNA and intrathecal inflammation.
AIDS
PUBLISHED: 03-20-2010
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A subset of HIV-infected patients, termed elite viral controllers, maintain undetectable plasma HIV RNA levels in the absence of therapy. In this group, host-mediated viral control may be accompanied by chronic systemic inflammation. It is unknown whether either infection or chronic inflammation is present within the central nervous system of these individuals.
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Cerebrospinal fluid neopterin: an informative biomarker of central nervous system immune activation in HIV-1 infection.
AIDS Res Ther
PUBLISHED: 02-25-2010
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HIV-1 invades the central nervous system (CNS) in the context of acute infection, persists thereafter in the absence of treatment, and leads to chronic intrathecal immunoactivation that can be measured by the macrophage activation marker, neopterin, in cerebrospinal fluid (CSF). In this review we describe our experience with CSF neopterin measurements in 382 untreated HIV-infected patients across the spectrum of immunosuppression and HIV-related neurological diseases, in 73 untreated AIDS patients with opportunistic CNS infections, and in 233 treated patients.In untreated patients, CSF neopterin concentrations are almost always elevated and increase progressively as immunosuppression worsens and blood CD4 cell counts fall. However, patients with HIV dementia exhibit particularly high CSF neopterin concentrations, above those of patients without neurological disease, though patients with CNS opportunistic infections, including CMV encephalitis and cryptococcal meningitis, also exhibit high levels of CSF neopterin. Combination antiretroviral therapy, with its potent effect on CNS HIV infection and CSF HIV RNA, mitigates both intrathecal immunoactivation and lowers CSF neopterin. However, despite suppression of plasma and CSF HIV RNA to below the detection limits of clinical assays (<50 copies HIV RNA/mL), CSF neopterin often remains mildly elevated, indicating persistent low-level intrathecal immune activation and raising the important questions of whether this elevation is driven by continued CNS infection and whether it causes continued indolent CNS injury.Although nonspecific, CSF neopterin can serve as a useful biomarker in the diagnosis of HIV dementia in the setting of confounding conditions, in monitoring the CNS inflammatory effects of antiretroviral treatment, and give valuable information to the cause of ongoing brain injury.
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Compartmentalization and clonal amplification of HIV-1 variants in the cerebrospinal fluid during primary infection.
J. Virol.
PUBLISHED: 12-16-2009
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Human immunodeficiency virus type 1 (HIV-1)-associated dementia (HAD) is a severe neurological disease that affects a subset of HIV-1-infected individuals. Increased compartmentalization has been reported between blood and cerebrospinal fluid (CSF) HIV-1 populations in subjects with HAD, but it is still not known when compartmentalization arises during the course of infection. To assess HIV-1 genetic compartmentalization early during infection, we compared HIV-1 populations in the peripheral blood and CSF in 11 primary infection subjects, with analysis of longitudinal samples over the first 18 months for a subset of subjects. We used heteroduplex tracking assays targeting the variable regions of env and single-genome amplification and sequence analysis of the full-length env gene to identify CSF-compartmentalized variants and to examine viral genotypes within the compartmentalized populations. For most subjects, HIV-1 populations were equilibrated between the blood and CSF compartments. However, compartmentalized HIV-1 populations were detected in the CSF of three primary infection subjects, and longitudinal analysis of one subject revealed that compartmentalization during primary HIV-1 infection was resolved. Clonal amplification of specific HIV-1 variants was identified in the CSF population of one primary infection subject. Our data show that compartmentalization can occur in the central nervous system (CNS) of subjects in primary HIV-1 infection in part through persistence of the putative transmitted parental variant or via viral genetic adaptation to the CNS environment. The presence of distinct HIV-1 populations in the CSF indicates that independent HIV-1 replication can occur in the CNS, even early after HIV-1 transmission.
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Amyloid and tau cerebrospinal fluid biomarkers in HIV infection.
BMC Neurol
PUBLISHED: 07-31-2009
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Because of the emerging intersections of HIV infection and Alzheimers disease, we examined cerebrospinal fluid (CSF) biomarkers related of amyloid and tau metabolism in HIV-infected patients.
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Raltegravir cerebrospinal fluid concentrations in HIV-1 infection.
PLoS ONE
PUBLISHED: 03-23-2009
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Raltegravir is an HIV-1 integrase inhibitor currently used in treatment-experienced HIV-1-infected patients resistant to other drug classes. In order to assess its central nervous system penetration, we measured raltegravir concentrations in cerebrospinal fluid (CSF) and plasma in subjects receiving antiretroviral treatment regimens containing this drug.
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Compartmentalized human immunodeficiency virus type 1 originates from long-lived cells in some subjects with HIV-1-associated dementia.
PLoS Pathog.
PUBLISHED: 01-26-2009
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Human immunodeficiency virus type 1 (HIV-1) invades the central nervous system (CNS) shortly after systemic infection and can result in the subsequent development of HIV-1-associated dementia (HAD) in a subset of infected individuals. Genetically compartmentalized virus in the CNS is associated with HAD, suggesting autonomous viral replication as a factor in the disease process. We examined the source of compartmentalized HIV-1 in the CNS of subjects with HIV-1-associated neurological disease and in asymptomatic subjects who were initiating antiretroviral therapy. The heteroduplex tracking assay (HTA), targeting the variable regions of env, was used to determine which HIV-1 genetic variants in the cerebrospinal fluid (CSF) were compartmentalized and which variants were shared with the blood plasma. We then measured the viral decay kinetics of individual variants after the initiation of antiretroviral therapy. Compartmentalized HIV-1 variants in the CSF of asymptomatic subjects decayed rapidly after the initiation of antiretroviral therapy, with a mean half-life of 1.57 days. Rapid viral decay was also measured for CSF-compartmentalized variants in four HAD subjects (t(1/2) mean = 2.27 days). However, slow viral decay was measured for CSF-compartmentalized variants from an additional four subjects with neurological disease (t(1/2) range = 9.85 days to no initial decay). The slow decay detected for CSF-compartmentalized variants was not associated with poor CNS drug penetration, drug resistant virus in the CSF, or the presence of X4 virus genotypes. We found that the slow decay measured for CSF-compartmentalized variants in subjects with neurological disease was correlated with low peripheral CD4 cell count and reduced CSF pleocytosis. We propose a model in which infiltrating macrophages replace CD4(+) T cells as the primary source of productive viral replication in the CNS to maintain high viral loads in the CSF in a substantial subset of subjects with HAD.
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Change in brain magnetic resonance spectroscopy after treatment during acute HIV infection.
PLoS ONE
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Single voxel proton magnetic resonance spectroscopy (MRS) can be used to monitor changes in brain inflammation and neuronal integrity associated with HIV infection and its treatments. We used MRS to measure brain changes during the first weeks following HIV infection and in response to antiretroviral therapy (ART).
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Neurologic complications of HIV infection.
Top Antivir Med
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The effects of HIV-1 in the nervous system are a topic of avid interest to investigators and clinicians focused on HIV, judging by the large and discriminating audience at the oral sessions and poster presentations relating to neuroscience at the 19th Conference on Retroviruses and Opportunistic Infections. Major areas of investigation at this years conference included the use of neuropsychological testing and neuroimaging to assess the state of the central nervous system (CNS) and effects of antiretroviral therapy during HIV infection as well as basic and clinical studies of neuropathogenesis of HIV-associated neurocognitive disorder (HAND). Numerous important suggestions emerged during the meeting. Among them was the proposition that earlier initiation of therapy might benefit the CNS. Another was that the relationship between HIV and normal aging remains unclear and warrants further study. Still another was that ongoing abnormalities may persist despite treatment with antiretroviral therapy-including measurable brain microglial activation, detectable cerebrospinal fluid HIV, and progression of neurologic impairment.
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HIV-1-related central nervous system disease: current issues in pathogenesis, diagnosis, and treatment.
Cold Spring Harb Perspect Med
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HIV-associated central nervous system (CNS) injury continues to be clinically significant in the modern era of HIV infection and therapy. A substantial proportion of patients with suppressed HIV infection on optimal antiretroviral therapy have impaired performance on neuropsychological testing, suggesting persistence of neurological abnormalities despite treatment and projected long-term survival. In the underresourced setting, limited accessibility to antiretroviral medications means that CNS complications of later-stage HIV infection continue to be a major concern. This article reviews key recent advances in our understanding of the neuropathogenesis of HIV, focusing on basic and clinical studies that reveal viral and host features associated with viral neuroinvasion, persistence, and immunopathogenesis in the CNS, as well as issues related to monitoring and treatment of HIV-associated CNS injury in the current era.
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Cerebrospinal fluid HIV escape associated with progressive neurologic dysfunction in patients on antiretroviral therapy with well controlled plasma viral load.
AIDS
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To characterize HIV-infected patients with neurosymptomatic cerebrospinal fluid (CSF) escape, defined as detectable CSF HIV RNA in the setting of treatment-suppressed plasma levels or CSF RNA more than 1-log higher than plasma RNA.
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Central nervous system viral invasion and inflammation during acute HIV infection.
J. Infect. Dis.
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Understanding the earliest central nervous system (CNS) events during human immunodeficiency virus (HIV) infection is crucial to knowledge of neuropathogenesis, but these have not previously been described in humans.
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The cerebrospinal fluid proteome in HIV infection: change associated with disease severity.
Clin Proteomics
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Central nervous system (CNS) infection is a nearly universal feature of untreated systemic HIV infection with a clinical spectrum that ranges from chronic asymptomatic infection to severe cognitive and motor dysfunction. Analysis of cerebrospinal fluid (CSF) has played an important part in defining the character of this evolving infection and response to treatment. To further characterize CNS HIV infection and its effects, we applied advanced high-throughput proteomic methods to CSF to identify novel proteins and their changes with disease progression and treatment.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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