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[PMID]: 28449599
[Au] Autor:Weikum D; Shrestha R; Ferro EG; Vagenas P; Copenhaver M; Spudich S; Alpert MD; Cabello R; Lama JR; Sanchez J; Altice FL
[Ad] Address:a Section of Infectious Diseases, AIDS Program , Yale School of Medicine , New Haven , CT , USA.
[Ti] Title:An explanatory factor analysis of a brief self-report scale to detect neurocognitive impairment among HIV-positive men who have sex with men and transgender women in Peru.
[So] Source:AIDS Care;29(10):1297-1301, 2017 Oct.
[Is] ISSN:1360-0451
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Neurocognitive impairment (NCI) has been associated with poor clinical outcomes in various patient populations. This study used exploratory factor analysis (EFA) to examine the factor structure of the existing 95-item Neuropsychological Impairment Scale (NIS) to create a suitable NCI screening instrument for people living with HIV (PLH). In Lima, Peru, 313 HIV-positive men who have sex with men (MSM) and transgender women (TGW) prescribed antiretroviral therapy (ART) completed the NIS using computer-assisted self-interviews (CASI). The EFA used principal axis factoring and orthogonal varimax rotation, which resulted in 42 items with an 8-factor solution that explained 51.8% of the overall variance. The revised, 8-factor, Brief Inventory of Neurocognitive Impairment for Peru (BINI-P) showed a diverse set of factors with excellent to good reliability (i.e., F α = 0.92 to F α = 0.78). This EFA supports the use of the BINI-P to screen for NCI among Spanish-speaking, HIV-positive MSM and TGW. Future research should examine the effectiveness of the BINI-P in detecting NCI in clinical care settings and the impact of NCI on HIV health-related outcomes, including linkage and retention in care, ART adherence and HIV risk behaviors.
[Mh] MeSH terms primary: HIV Infections/psychology
Homosexuality, Male/psychology
Neurocognitive Disorders/diagnosis
Neuropsychological Tests
Transgender Persons/psychology
[Mh] MeSH terms secundary: Adult
Factor Analysis, Statistical
Female
HIV Infections/drug therapy
Humans
Male
Neurocognitive Disorders/psychology
Peru
Reproducibility of Results
Self Report
Surveys and Questionnaires
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM; X
[Da] Date of entry for processing:170429
[St] Status:MEDLINE
[do] DOI:10.1080/09540121.2017.1322681

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[PMID]: 29221753
[Au] Autor:Daniel DC; Johnson EM
[Ad] Address:Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA 23507, USA.
[Ti] Title:PURA, the gene encoding Pur-alpha, member of an ancient nucleic acid-binding protein family with mammalian neurological functions.
[So] Source:Gene;643:133-143, 2018 Feb 15.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The PURA gene encodes Pur-alpha, a 322 amino acid protein with repeated nucleic acid binding domains that are highly conserved from bacteria through humans. PUR genes with a single copy of this domain have been detected so far in spirochetes and bacteroides. Lower eukaryotes possess one copy of the PUR gene, whereas chordates possess 1 to 4 PUR family members. Human PUR genes encode Pur-alpha (Pura), Pur-beta (Purb) and two forms of Pur-gamma (Purg). Pur-alpha is a protein that binds specific DNA and RNA sequence elements. Human PURA, located at chromosome band 5q31, is under complex control of three promoters. The entire protein coding sequence of PURA is contiguous within a single exon. Several studies have found that overexpression or microinjection of Pura inhibits anchorage-independent growth of oncogenically transformed cells and blocks proliferation at either G1-S or G2-M checkpoints. Effects on the cell cycle may be mediated by interaction of Pura with cellular proteins including Cyclin/Cdk complexes and the Rb tumor suppressor protein. PURA knockout mice die shortly after birth with effects on brain and hematopoietic development. In humans environmentally induced heterozygous deletions of PURA have been implicated in forms of myelodysplastic syndrome and progression to acute myelogenous leukemia. Pura plays a role in AIDS through association with the HIV-1 protein, Tat. In the brain Tat and Pura association in glial cells activates transcription and replication of JC polyomavirus, the agent causing the demyelination disease, progressive multifocal leukoencephalopathy. Tat and Pura also act to stimulate replication of the HIV-1 RNA genome. In neurons Pura accompanies mRNA transcripts to sites of translation in dendrites. Microdeletions in the PURA locus have been implicated in several neurological disorders. De novo PURA mutations have been related to a spectrum of phenotypes indicating a potential PURA syndrome. The nucleic acid, G-rich Pura binding element is amplified as expanded polynucleotide repeats in several brain diseases including fragile X syndrome and a familial form of amyotrophic lateral sclerosis/fronto-temporal dementia. Throughout evolution the Pura protein plays a critical role in survival, based on conservation of its nucleic acid binding properties. These Pura properties have been adapted in higher organisms to the as yet unfathomable development of the human brain.
[Mh] MeSH terms primary: DNA-Binding Proteins/genetics
DNA-Binding Proteins/metabolism
Transcription Factors/genetics
Transcription Factors/metabolism
[Mh] MeSH terms secundary: Amino Acid Sequence/genetics
Animals
Base Sequence
Cell Cycle
Cell Cycle Proteins/genetics
Conserved Sequence/genetics
DNA Replication
Dendritic Cells/metabolism
HIV-1/genetics
Humans
Leukemia, Myeloid, Acute/genetics
Myelodysplastic Syndromes/genetics
Neuroglia/metabolism
Neurons/metabolism
RNA Recognition Motif Proteins/genetics
RNA Recognition Motif Proteins/metabolism
RNA, Messenger/metabolism
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Cell Cycle Proteins); 0 (DNA-Binding Proteins); 0 (PURA protein, human); 0 (RNA Recognition Motif Proteins); 0 (RNA, Messenger); 0 (Transcription Factors)
[Em] Entry month:1801
[Cu] Class update date: 180210
[Lr] Last revision date:180210
[Js] Journal subset:IM
[Da] Date of entry for processing:171210
[St] Status:MEDLINE

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[PMID]: 29292194
[Au] Autor:Singh H; Samani D; Nambiar N; Ghate MV; Gangakhedkar RR
[Ad] Address:Department of Molecular Biology, National AIDS Research Institute, Pune 411026, India. Electronic address: hsingh@nariindia.org.
[Ti] Title:Prevalence of MMP-8 gene polymorphisms in HIV-infected individuals and its association with HIV-associated neurocognitive disorder.
[So] Source:Gene;646:83-90, 2018 Mar 10.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Matrix metalloproteinases (MMPs) are well-known as mediators of neuroinflammation in HIV-associated neurocognitive disorder (HAND). Increased levels of MMP-8 have been observed in the HIV-infected patients. Thus, the aim of this study was to evaluate the association of MMP-8 gene polymorphisms with modulation of HAND severity and its prevalence in HIV-infected and healthy individuals. We enrolled a total of 150 HIV-infected individuals, 50 HAND patients, 100 HIV-infected and 150 healthy individuals. MMP-8 (-799C/T, +17C/G) polymorphisms were genotyped by PCR-RFLP. MMP-8 -799TT genotype and +17G allele showed the higher risk for modulation of HAND severity (OR=2.20, P=0.19; OR=1.97, P=0.23). MMP-8 -799TT genotype differed significantly in HIV-infected individuals compared to healthy controls (20.0% vs. 11.3%, OR=2.36, P=0.048). Haplotype TG increased the risk for modulation of HAND severity (OR=2.29, P=0.29). MMP-8 -799TT and +17CG genotypes were overrepresented in the intermediate HIV disease stage compared with healthy controls (25.9% vs. 11.3%, OR=4.34, P=0.021, 14.8% vs. 9.3%, OR=2.88, P=0.11). MMP-8 +17CG genotype enhanced the risk for modulation of HAND severity in tobacco using HAND patients (OR=5.01, P=0.17). MMP-8 -799TT genotype was more frequent in tobacco using HIV-infected individuals compared with nonusers (26.3% vs. 16.7%, OR=2.08, P=0.32). MMP-8 +17CG genotype increased the risk for modulation of HAND severity in alcohol using HAND patients (OR=4.99, P=0.18). In conclusion, MMP-8 polymorphisms independently and with alcohol and tobacco usage revealed a trend of higher risk for the modulation of HAND severity. MMP-8 -799TT genotype was associated with the advancement of HIV disease.
[Mh] MeSH terms primary: AIDS Dementia Complex/genetics
HIV Infections/genetics
Matrix Metalloproteinase 8/genetics
Polymorphism, Single Nucleotide
Up-Regulation
[Mh] MeSH terms secundary: Adult
Alcohols/adverse effects
Case-Control Studies
Female
Genetic Association Studies
Genetic Predisposition to Disease
Genotype
HIV Infections/complications
Haplotypes
Humans
Male
Prevalence
Promoter Regions, Genetic
Risk Factors
Severity of Illness Index
Smoking/adverse effects
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Alcohols); EC 3.4.24.34 (MMP8 protein, human); EC 3.4.24.34 (Matrix Metalloproteinase 8)
[Em] Entry month:1802
[Cu] Class update date: 180202
[Lr] Last revision date:180202
[Js] Journal subset:IM
[Da] Date of entry for processing:180103
[St] Status:MEDLINE

  4 / 4029 MEDLINE  
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[PMID]: 29323557
[Au] Autor:Gascón MRP; Vidal JE; Mazzaro YM; Smid J; Marcusso RMN; Capitão CG; Coutinho EM; Benute GRG; De Lucia MCS; de Oliveira ACP
[Ad] Address:1 Division of Psychology, Central Institute of Hospital das Clinicas , Faculdade de Medicina de São Paulo, São Paulo, Brazil .
[Ti] Title:Neuropsychological Assessment of 412 HIV-Infected Individuals in São Paulo, Brazil.
[So] Source:AIDS Patient Care STDS;32(1):1-8, 2018 Jan.
[Is] ISSN:1557-7449
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:HIV-associated neurocognitive disorders (HAND) remain frequent even among individuals receiving combined antiretroviral therapy (cART). In addition, HAND may adversely affect the quality of life and adherence to cART. There is scarce epidemiological information about HAND in Latin America. This cross-sectional study recruited HIV-infected patients from a tertiary teaching institution in São Paulo, Brazil, between May 2013 and February 2015. The patients were adults with at least 4 years of education and patients with current neurological or psychiatric diseases were excluded. HAND remain frequent even among individuals receiving cART, use of psychoactive substance, or inability to understand the content for neuropsychological evaluation. We used standardized tools to evaluate depression, use of psychoactive substances, and daily life activities, and we performed a comprehensive neuropsychological examination. HAND was classified using the Frascati criteria. Prevalence of HAND was estimated, and an associated variable of symptomatic HAND was identified by logistic regression. Four-hundred twelve HIV-infected patients were included [male: 281 (68%), mean age of 45.3 years]. Most of them [n = 340 (83.7%)] had an undetectable viral load. The prevalence of HAND was 73.6% (n = 303): 210 (50.9%) had asymptomatic neurocognitive involvement (ANI), 67 (16.2%) had mild neurocognitive disorder (MND), and 26 (6.3%) had HIV-associated dementia (HAD). The univariate logistic regression analysis showed that female gender, age older than 50 years, <11 years of schooling, CD4 count below 200 cells/mm , presence of previous illnesses (e.g., diabetes, hypertension), opportunistic disease history, and a Beck Depression Inventory (BDI) score between 13 and 19 points were factors associated with symptomatic HAND (MND and HAD). However, a BDI score between 13 and 19 points was the single independent variable associated with symptomatic HAND. HAND was highly prevalent in São Paulo, Brazil, and ANI was the more frequent category of HAND. However, 22.5% of participants had symptomatic HAND. This finding constitutes a challenge in clinical practice. A BDI score between 13 and 19 points was the single independent variable associated with symptomatic HAND.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180111
[Lr] Last revision date:180111
[St] Status:In-Data-Review
[do] DOI:10.1089/apc.2017.0202

  5 / 4029 MEDLINE  
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[PMID]: 28929901
[Au] Autor:Parke B; Hunter KF
[Ad] Address:1 Faculty of Nursing, Edmonton Clinic Health Academy, University of Alberta, Edmonton, Alberta, Canada.
[Ti] Title:The dementia-friendly emergency department: An innovation to reducing incompatibilities at the local level.
[So] Source:Healthc Manage Forum;30(1):26-31, 2017 Jan.
[Is] ISSN:0840-4704
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Emergency Departments (EDs) are an integral part of the Canadian healthcare system. Older people living with dementia challenge EDs. They have complex health profiles that pose multiple challenges for staff. The current one-size-fits-all approach that aids efficiency in a technologically dependent hospital setting may not always serve older people living with dementia, their caregivers, or staff well. The premise that older people living with dementia are a problem for Canadian EDs must be reconsidered. Understanding the complexity of the situation is aided by the dementia-friendly ED framework. We propose one way to enhance communication between those living with dementia who receive ED services and those providing the service.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1709
[Cu] Class update date: 170920
[Lr] Last revision date:170920
[St] Status:In-Data-Review
[do] DOI:10.1177/0840470416664532

  6 / 4029 MEDLINE  
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[PMID]: 28814330
[Au] Autor:Allemann SS; Dürsteler KM; Strasser J; Vogel M; Stoeckle M; Hersberger KE; Arnet I
[Ad] Address:Pharmaceutical Care Research Group, Pharmaceutical Sciences, University of Basel, Basel, Switzerland. s.allemann@unibas.ch.
[Ti] Title:Novel remote electronic medication supply model for opioid-dependent outpatients with polypharmacy--first long-term case study.
[So] Source:Harm Reduct J;14(1):56, 2017 Aug 16.
[Is] ISSN:1477-7517
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Patients with substance use disorders grow older thanks to effective treatments. Together with a high prevalence of comorbidities, psychological problems, and low social support, these patients are at high risk for medication non-adherence. Established treatment facilities face challenges to accommodate these complex patients within their setting. Electronic medication management aids (e-MMAs) might be appropriate to simultaneously monitor and improve adherence for these patients. CASE PRESENTATION: We report the first long-term experiences with a novel remote electronic medication supply model for two opioid-dependent patients with HIV. John (beginning dementia, 52 years, 6 tablets daily at 12 am) and Mary (frequent drug holidays, 48 years, 5-6 tablets daily at 8 pm) suffered from disease progression due to non-adherence. We electronically monitored adherence and clinical outcomes during 659 (John) and 953 (Mary) days between July 2013 and April 2016. Both patients retrieved over 90% of the pouches within 75 min of the scheduled time. Technical problems occurred in 4% (John) and 7.2% (Mary) of retrievals, but on-site support was seldom required. Viral loads fell below detection limits during the entire observation period. CONCLUSIONS: Continuous medication supply and persistence with treatment of over 1.7 years, timing adherence of more than 90%, and suppressed HIV viral load are first results supporting the feasibility of the novel supply model for patients on opioid-assisted treatment and polypharmacy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1708
[Cu] Class update date: 170821
[Lr] Last revision date:170821
[St] Status:In-Process
[do] DOI:10.1186/s12954-017-0182-x

  7 / 4029 MEDLINE  
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[PMID]: 28797021
[Au] Autor:Yuen T; Brouillette MJ; Fellows LK; Ellis RJ; Letendre S; Heaton R; Mayo N; CHARTER group,
[Ad] Address:*Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Québec, Canada;†Division of Clinical Epidemiology, McGill University Health Center, Montreal, Québec, Canada;‡Chronic Viral Illness Service, McGill University Health Centre and Department of Psychiatry, McGill University, Montreal, Québec, Canada;§Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Québec, Canada;Departments of ‖Neurosciences; and¶Psychiatry, University of California San Diego, San Diego, CA; and#HIV Neurobehavioural Research Centre, University of California San Diego, San Diego, CA.
[Ti] Title:Personalized Risk Index for Neurocognitive Decline Among People With Well-Controlled HIV Infection.
[So] Source:J Acquir Immune Defic Syndr;76(1):48-54, 2017 Sep 01.
[Is] ISSN:1944-7884
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Little is known about the predictors of neurocognitive decline in HIV+ individuals with good virological control. Identification of modifiable risk factors would allow targeted interventions to reduce the risk of decline in higher risk individuals. The objective of this study was to develop a risk index to predict neurocognitive decline over 3 years in aviremic HIV+ individuals. METHODS: As part of the CNS HIV Anti-Retroviral Therapy Effects Research (CHARTER) study, HIV+ adults completed clinical evaluation and neuropsychological tests every 6 months. Group-based trajectory analysis was used to detect patterns of neurocognitive change; individuals who deteriorated ≥ 0.5 SD on at least one neuropsychological test were considered decliners. Multiple logistic regression was used to identify baseline sociodemographic, clinical, biological, and lifestyle factors associated with decline in the subgroup that was consistently aviremic during the first 3 years. A risk index was developed using the beta-coefficients from the final regression model. RESULTS: Neurocognitive decline occurred in 23 of 191 (12%) participants followed longitudinally. The baseline factors that predicted decline were glomerular filtration rate ≤50 mL/min, known duration of HIV infection ≥15 years, education ≤12 years, and cerebrospinal fluid protein >45 mg/dL. CONCLUSIONS: Using this analytic approach, neurocognitive decline was uncommon in this sample of aviremic HIV+ individuals. The 3-year risk of decline ranged from 2% in those with no risk factors to 95% in those with all 4. The strongest predictor was glomerular filtration rate, also a predictor of cardiovascular disease. This raises the possibility that controlling vascular risk factors could reduce the risk of neurocognitive decline.
[Mh] MeSH terms primary: AIDS Dementia Complex/physiopathology
Cardiovascular Diseases/physiopathology
HIV Infections/physiopathology
[Mh] MeSH terms secundary: Adult
Antiretroviral Therapy, Highly Active
Cardiovascular Diseases/virology
Educational Status
Female
Follow-Up Studies
Glomerular Filtration Rate
HIV Infections/complications
Humans
Longitudinal Studies
Male
Middle Aged
Neuropsychological Tests
Risk Factors
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171030
[Lr] Last revision date:171030
[Js] Journal subset:IM; X
[Da] Date of entry for processing:170811
[St] Status:MEDLINE
[do] DOI:10.1097/QAI.0000000000001466

  8 / 4029 MEDLINE  
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[PMID]: 28792504
[Au] Autor:Sagar V; Pilakka-Kanthikeel S; Martinez PC; Atluri VSR; Nair M
[Ad] Address:Institute of Neuroimmune Pharmacology/Center for Personalized Nanomedicine, Department of Immunology, Herbert Wertheim College of Medicine, Florida International University, Miami, Florida, United States of America.
[Ti] Title:Common gene-network signature of different neurological disorders and their potential implications to neuroAIDS.
[So] Source:PLoS One;12(8):e0181642, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The neurological complications of AIDS (neuroAIDS) during the infection of human immunodeficiency virus (HIV) are symptomized by non-specific, multifaceted neurological conditions and therefore, defining a specific diagnosis/treatment mechanism(s) for this neuro-complexity at the molecular level remains elusive. Using an in silico based integrated gene network analysis we discovered that HIV infection shares convergent gene networks with each of twelve neurological disorders selected in this study. Importantly, a common gene network was identified among HIV infection, Alzheimer's disease, Parkinson's disease, multiple sclerosis, and age macular degeneration. An mRNA microarray analysis in HIV-infected monocytes showed significant changes in the expression of several genes of this in silico derived common pathway which suggests the possible physiological relevance of this gene-circuit in driving neuroAIDS condition. Further, this unique gene network was compared with another in silico derived novel, convergent gene network which is shared by seven major neurological disorders (Alzheimer's disease, Parkinson's disease, Multiple Sclerosis, Age Macular Degeneration, Amyotrophic Lateral Sclerosis, Vascular Dementia, and Restless Leg Syndrome). These networks differed in their gene circuits; however, in large, they involved innate immunity signaling pathways, which suggests commonalities in the immunological basis of different neuropathogenesis. The common gene circuits reported here can provide a prospective platform to understand how gene-circuits belonging to other neuro-disorders may be convoluted during real-time neuroAIDS condition and it may elucidate the underlying-and so far unknown-genetic overlap between HIV infection and neuroAIDS risk. Also, it may lead to a new paradigm in understanding disease progression, identifying biomarkers, and developing therapies.
[Mh] MeSH terms primary: AIDS Dementia Complex/genetics
AIDS Dementia Complex/metabolism
Gene Regulatory Networks
Nervous System Diseases/genetics
Nervous System Diseases/metabolism
[Mh] MeSH terms secundary: Cell Line
Computational Biology
HIV-1
Humans
Microarray Analysis
Monocytes/metabolism
RNA, Messenger/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (RNA, Messenger)
[Em] Entry month:1710
[Cu] Class update date: 171006
[Lr] Last revision date:171006
[Js] Journal subset:IM
[Da] Date of entry for processing:170810
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181642

  9 / 4029 MEDLINE  
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[PMID]: 28787449
[Au] Autor:Matsuda K; Riddick NE; Lee CA; Puryear SB; Wu F; Lafont BAP; Whitted S; Hirsch VM
[Ad] Address:Laboratory of Molecular Microbiology, NIAID, NIH, Bethesda, MD, United States of America.
[Ti] Title:A SIV molecular clone that targets the CNS and induces neuroAIDS in rhesus macaques.
[So] Source:PLoS Pathog;13(8):e1006538, 2017 Aug.
[Is] ISSN:1553-7374
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Despite effective control of plasma viremia with the use of combination antiretroviral therapies (cART), minor cognitive and motor disorders (MCMD) persist as a significant clinical problem in HIV-infected patients. Non-human primate models are therefore required to study mechanisms of disease progression in the central nervous system (CNS). We isolated a strain of simian immunodeficiency virus (SIV), SIVsm804E, which induces neuroAIDS in a high proportion of rhesus macaques and identified enhanced antagonism of the host innate factor BST-2 as an important factor in the macrophage tropism and initial neuro-invasion of this isolate. In the present study, we further developed this model by deriving a molecular clone SIVsm804E-CL757 (CL757). This clone induced neurological disorders in high frequencies but without rapid disease progression and thus is more reflective of the tempo of neuroAIDS in HIV-infection. NeuroAIDS was also induced in macaques co-inoculated with CL757 and the parental AIDS-inducing, but non-neurovirulent SIVsmE543-3 (E543-3). Molecular analysis of macaques infected with CL757 revealed compartmentalization of virus populations between the CNS and the periphery. CL757 exclusively targeted the CNS whereas E543-3 was restricted to the periphery consistent with a role for viral determinants in the mechanisms of neuroinvasion. CL757 would be a useful model to investigate disease progression in the CNS and as a model to study virus reservoirs in the CNS.
[Mh] MeSH terms primary: AIDS Dementia Complex/virology
Disease Models, Animal
Simian Acquired Immunodeficiency Syndrome/genetics
Simian Immunodeficiency Virus/genetics
[Mh] MeSH terms secundary: Animals
Brain/virology
Flow Cytometry
Macaca mulatta
Polymerase Chain Reaction
Simian Acquired Immunodeficiency Syndrome/complications
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171003
[Lr] Last revision date:171003
[Js] Journal subset:IM
[Da] Date of entry for processing:170809
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006538

  10 / 4029 MEDLINE  
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[PMID]: 28762691
[Au] Autor:Chu C; Pollock LC; Selwyn PA
[Ad] Address:University of California at San Francisco School of Medicine, San Francisco, CA, USA.
[Ti] Title:HIV-Associated Complications: A Systems-Based Approach.
[So] Source:Am Fam Physician;96(3):161-169, 2017 Aug 01.
[Is] ISSN:1532-0650
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Persons with human immunodeficiency virus (HIV) infection often develop complications related directly to the infection, as well as to treatment. Aging, lifestyle factors, and comorbidities increase the risk of developing chronic conditions such as diabetes mellitus and chronic kidney disease. HIV-associated neurologic complications encompass a wide spectrum of pathophysiology and symptomatology. Cardiovascular and pulmonary conditions are common among persons with HIV infection. Although some specific antiretroviral medications have been linked to disease development, traditional risk factors (e.g., smoking) have major roles. Prevention and management of viral hepatitis coinfection are important to reduce morbidity and mortality, and new anti-hepatitis C agents produce high rates of sustained virologic response. Antiretroviral-associated metabolic complications include dyslipidemia, hyperglycemia, and loss of bone mineral density. Newer options generally pose less risk of significant systemic toxicity and are better tolerated. Family physicians who care for patients with HIV infection have a key role in identifying and managing many of these chronic complications.
[Mh] MeSH terms primary: HIV Infections/complications
[Mh] MeSH terms secundary: AIDS Dementia Complex/diagnosis
Cardiovascular Diseases/diagnosis
Cardiovascular Diseases/etiology
HIV Enteropathy/diagnosis
Humans
Metabolic Diseases/diagnosis
Metabolic Diseases/etiology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1708
[Cu] Class update date: 170807
[Lr] Last revision date:170807
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170802
[St] Status:MEDLINE


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