LIVIVO - Search results -

Search results

Result 1 - 10 of total 18

Search options

Article ; Online: Innate immune responses reverse HIV cognitive disease in mice: Profile by RNAseq in the brain.

Borjabad, Alejandra / Dong, Baojun / Chao, Wei / Volsky, David J / Potash, Mary Jane

2023 Volume 589, Page(s) 109917

Abstract: Antiretroviral therapy controls immunodeficiency in people with HIV but many develop mild neurocognitive disorder. Here we investigated HIV brain disease by infecting mice with the chimeric HIV, EcoHIV, and probing changes in brain gene expression during ...

Abstract	Antiretroviral therapy controls immunodeficiency in people with HIV but many develop mild neurocognitive disorder. Here we investigated HIV brain disease by infecting mice with the chimeric HIV, EcoHIV, and probing changes in brain gene expression during infection and reversal with polyinosinic-polycytidylic acid (poly I:C). EcoHIV-infected C57BL/6 mice were treated with poly I:C and monitored by assay of learning in radial arm water maze, RNAseq of striatum, and QPCR of virus burden and brain transcripts. Poly I:C reversed EcoHIV-associated cognitive impairment and reduced virus burden. Major pathways downregulated by infection involved neuronal function, these transcriptional changes were normalized by poly I:C treatment. Innate immune responses were the major pathways induced in EcoHIV-infected, poly I:C treated mice. Our findings provide a framework to identify brain cell genes dysregulated by HIV infection and identify a set of innate immune response genes that can block systemic infection and its associated dysfunction in the brain.
MeSH term(s)	Humans ; Animals ; Mice ; HIV Infections/complications ; Mice, Inbred C57BL ; Brain ; Immunity, Innate ; Cognition ; Poly I
Chemical Substances	Poly I (25249-22-3)
Language	English
Publishing date	2023-11-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2023.109917
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.172: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Prevention and treatment of HIV infection and cognitive disease in mice by innate immune responses.

Dong, Baojun / Borjabad, Alejandra / Kelschenbach, Jennifer / Chao, Wei / Volsky, David J / Potash, Mary Jane

Brain, behavior, & immunity - health

2020 Volume 3

Abstract: HIV associated neurocognitive impairment afflicts roughly half of infected individuals on antiretroviral therapy. This disease currently has no treatment. We have previously shown that type I interferon is induced by and partially controls infection and ... ...

Abstract	HIV associated neurocognitive impairment afflicts roughly half of infected individuals on antiretroviral therapy. This disease currently has no treatment. We have previously shown that type I interferon is induced by and partially controls infection and neuropathogenesis in mice infected by chimeric HIV, EcoHIV. Here we investigate the intentional ligation of the pattern recognition receptor Toll-like receptor 3 (TLR3) by polyinosinic-polycytidylic acid (poly I:C) for its ability to prevent or control infection and associated cognitive disease in EcoHIV infected mice. We tested topical, injection, and intranasal application of poly I:C in mice during primary infection through injection or sexual transmission or in established infection. We measured different forms of HIV DNA and RNA in tissues by real-time PCR and the development of HIV-associated cognitive disease by the radial arm water maze behavioral test. Our results indicate that poly I:C blocks primary EcoHIV infection of mice prior to reverse transcription and reduces established EcoHIV infection. Prevention or control of viral replication by poly I:C prevents or reverses HIV associated cognitive disease in mice. These findings indicate that poly I:C or other innate immune agonists may be useful in control of HIV cognitive disease.
Language	English
Publishing date	2020-02-23
Publishing country	United States
Document type	Journal Article
ISSN	2666-3546
ISSN (online)	2666-3546
DOI	10.1016/j.bbih.2020.100054
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

Article ; Online: Neutral sphingomyelinase 2 inhibition attenuates extracellular vesicle release and improves neurobehavioral deficits in murine HIV.

Zhu, Xiaolei / Hollinger, Kristen R / Huang, Yiyao / Borjabad, Alejandra / Kim, Boe-Hyun / Arab, Tanina / Thomas, Ajit G / Moniruzzaman, Mohammed / Lovell, Lyndah / Turchinovich, Andrey / Witwer, Kenneth W / Volsky, David J / Haughey, Norman J / Slusher, Barbara S

Neurobiology of disease

2022 Volume 169, Page(s) 105734

Abstract: People living with HIV (PLH) have significantly higher rates of cognitive impairment (CI) and major depressive disorder (MDD) versus the general population. The enzyme neutral sphingomyelinase 2 (nSMase2) is involved in the biogenesis of ceramide and ... ...

Abstract	People living with HIV (PLH) have significantly higher rates of cognitive impairment (CI) and major depressive disorder (MDD) versus the general population. The enzyme neutral sphingomyelinase 2 (nSMase2) is involved in the biogenesis of ceramide and extracellular vesicles (EVs), both of which are dysregulated in PLH, CI, and MDD. Here we evaluated EcoHIV-infected mice for behavioral abnormalities relevant to depression and cognition deficits, and assessed the behavioral and biochemical effects of nSMase2 inhibition. Mice were infected with EcoHIV and daily treatment with either vehicle or the nSMase2 inhibitor (R)-(1-(3-(3,4-dimethoxyphenyl)-2,6-dimethylimidazo[1,2-b]pyridazin-8-yl)pyrrolidin-3-yl)-carbamate (PDDC) began 3 weeks post-infection. After 2 weeks of treatment, mice were subjected to behavior tests. EcoHIV-infected mice exhibited behavioral abnormalities relevant to MDD and CI that were reversed by PDDC treatment. EcoHIV infection significantly increased cortical brain nSMase2 activity, resulting in trend changes in sphingomyelin and ceramide levels that were normalized by PDDC treatment. EcoHIV-infected mice also exhibited increased levels of brain-derived EVs and altered microRNA cargo, including miR-183-5p, miR-200c-3p, miR-200b-3p, and miR-429-3p, known to be associated with MDD and CI; all were normalized by PDDC. In conclusion, inhibition of nSMase2 represents a possible new therapeutic strategy for the treatment of HIV-associated CI and MDD.
MeSH term(s)	Animals ; Ceramides ; Depressive Disorder, Major ; Extracellular Vesicles ; HIV Infections/complications ; HIV Infections/drug therapy ; Humans ; Mice ; MicroRNAs/genetics ; MicroRNAs/pharmacology ; Sphingomyelin Phosphodiesterase/genetics
Chemical Substances	Ceramides ; MicroRNAs ; Sphingomyelin Phosphodiesterase (EC 3.1.4.12)
Language	English
Publishing date	2022-04-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2022.105734
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4444: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Common transcriptional signatures in brain tissue from patients with HIV-associated neurocognitive disorders, Alzheimer's disease, and Multiple Sclerosis.

Borjabad, Alejandra / Volsky, David J

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2012 Volume 7, Issue 4, Page(s) 914–926

Abstract: HIV-Associated Neurocognitive Disorders (HAND) is a common manifestation of HIV infection that afflicts about 50 % of HIV-positive individuals. As people with access to antiretroviral treatments live longer, HAND can be found in increasing segments of ... ...

Abstract	HIV-Associated Neurocognitive Disorders (HAND) is a common manifestation of HIV infection that afflicts about 50 % of HIV-positive individuals. As people with access to antiretroviral treatments live longer, HAND can be found in increasing segments of populations at risk for other chronic, neurodegenerative conditions such as Alzheimer's disease (AD) and Multiple Sclerosis (MS). If brain diseases of diverse etiologies utilize similar biological pathways in the brain, they may coexist in a patient and possibly exacerbate neuropathogenesis and morbidity. To test this proposition, we conducted comparative meta-analysis of selected publicly available microarray datasets from brain tissues of patients with HAND, AD, and MS. In pair-wise and three-way analyses, we found a large number of dysregulated genes and biological processes common to either HAND and AD or HAND and MS, or to all three diseases. The common characteristic of all three diseases was up-regulation of broadly ranging immune responses in the brain. In addition, HAND and AD share down-modulation of processes involved, among others, in synaptic transmission and cell-cell signaling while HAND and MS share defective processes of neurogenesis and calcium/calmodulin-dependent protein kinase activity. Our approach could provide insight into the identification of common disease mechanisms and better intervention strategies for complex neurocognitive disorders.
MeSH term(s)	AIDS Dementia Complex/genetics ; AIDS Dementia Complex/immunology ; Alzheimer Disease/genetics ; Alzheimer Disease/immunology ; Antigen Presentation/genetics ; Brain Chemistry/genetics ; Frontal Lobe/chemistry ; Frontal Lobe/metabolism ; Gene Expression Profiling ; Genetic Markers/genetics ; Humans ; Microarray Analysis ; Multiple Sclerosis/genetics ; Multiple Sclerosis/immunology ; Transcription, Genetic/genetics ; Transcriptome/genetics
Chemical Substances	Genetic Markers
Language	English
Publishing date	2012-10-12
Publishing country	United States
Document type	Journal Article ; Meta-Analysis ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-012-9409-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: Lipid and lipoprotein parameters for detection of familial hypercholesterolemia in childhood. The DECOPIN Project.

Plana, Núria / Rodríguez-Borjabad, Cèlia / Ibarretxe, Daiana / Ferré, Raimon / Feliu, Albert / Caselles, Alejandra / Masana, Luis

Clinica e investigacion en arteriosclerosis : publicacion oficial de la Sociedad Espanola de Arteriosclerosis

2018 Volume 30, Issue 4, Page(s) 170–178

Abstract: Background: Familial hypercholesterolaemia (FH) in children is under-detected and is difficult to diagnose in clinical practice. The aim of this study was to evaluate clinical, biochemical and vascular imaging variables in order to detect children and ... ...

Title translation	Valor de los parámetros lipídicos y apoproteicos para la detección de hipercolesterolemia familiar en la infancia. Proyecto DECOPIN.
Abstract	Background: Familial hypercholesterolaemia (FH) in children is under-detected and is difficult to diagnose in clinical practice. The aim of this study was to evaluate clinical, biochemical and vascular imaging variables in order to detect children and adolescents with FH. Methods: A total of 222 children aged 4-18 years old were recruited to participate in a project for the early detection of FH (The DECOPIN Project). They were distributed into 3groups: FH, if genetic study or clinical criteria were positive (n=91); Polygenic hypercholesterolaemia (PH) if LDL-Cholesterol >135mg/dL without FH criteria (n=23), and Control group (CG) if LDL-C <135mg/dL (n=108). Data were collected from family history, anthropometric data, and clinical variables. The usual biochemical parameters, including a complete lipid profile were analysed. The carotid intima-media thickness (cIMT) and thickness of Achilles tendons were determined using ultrasound in all participants. Results: A total of 91 children had a diagnosis of FH, 23 with PH, and 108 with CG. Children with FH had higher concentrations of total cholesterol, LDL-C, ApoB/ApoA1 ratio, and cholesterol-year score, than the other groups. HDL-C was lower in the FH group than in the CG. Thickness of the Achilles tendon and cIMT did not show any differences between groups, although a greater cIMT trend was observed in the FH group. ApoB/ApoA1 ratio >0.82 was the parameter with the highest sensitivity and specificity to predict the presence of mutation in children with FH. Conclusions: Although LDL-C is the main biochemical parameter used to define FH, the ApoB/ApoA1 ratio (>0.82) may be a useful tool to identify children with FH and a positive mutation.
MeSH term(s)	Achilles Tendon/diagnostic imaging ; Adolescent ; Apolipoprotein A-I/blood ; Apolipoprotein B-100/blood ; Carotid Intima-Media Thickness ; Case-Control Studies ; Child ; Child, Preschool ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Female ; Humans ; Hypercholesterolemia/blood ; Hypercholesterolemia/diagnosis ; Hypercholesterolemia/genetics ; Hyperlipoproteinemia Type II/blood ; Hyperlipoproteinemia Type II/diagnosis ; Hyperlipoproteinemia Type II/genetics ; Lipids/blood ; Male ; Mutation ; Sensitivity and Specificity
Chemical Substances	APOA1 protein, human ; APOB protein, human ; Apolipoprotein A-I ; Apolipoprotein B-100 ; Cholesterol, HDL ; Cholesterol, LDL ; Lipids
Language	Spanish
Publishing date	2018-03-27
Publishing country	Spain
Document type	Journal Article
ISSN	1578-1879
ISSN (online)	1578-1879
DOI	10.1016/j.arteri.2017.12.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Efficient Expression of HIV in Immunocompetent Mouse Brain Reveals a Novel Nonneurotoxic Viral Function in Hippocampal Synaptodendritic Injury and Memory Impairment.

Kelschenbach, Jennifer / He, Hongxia / Kim, Boe-Hyun / Borjabad, Alejandra / Gu, Chao-Jiang / Chao, Wei / Do, Meilan / Sharer, Leroy R / Zhang, Hong / Arancio, Ottavio / Potash, Mary Jane / Volsky, David J

mBio

2019 Volume 10, Issue 4

Abstract: HIV causes neurodegeneration and dementia in AIDS patients, but its function in milder cognitive impairments in virologically suppressed patients on antiretroviral therapy is unknown. Such patients are immunocompetent, have low peripheral and brain HIV ... ...

Abstract	HIV causes neurodegeneration and dementia in AIDS patients, but its function in milder cognitive impairments in virologically suppressed patients on antiretroviral therapy is unknown. Such patients are immunocompetent, have low peripheral and brain HIV burdens, and show minimal brain neuropathology. Using the model of HIV-related memory impairment in EcoHIV-infected conventional mice, we investigated the neurobiological and cognitive consequences of efficient EcoHIV expression in the mouse brain after intracerebral infection. HIV integrated and persisted in an expressed state in brain tissue, was detectable in brain monocytic cells, and caused neuroinflammatory responses and lasting spatial, working, and associative memory impairment. Systemic antiretroviral treatment prevented direct brain infection and memory dysfunction indicating the requirement for HIV expression in the brain for disease. Similarly inoculated murine leukemia virus used as a control replicated in mouse brain but not in monocytic cells and was cognitively benign, linking the disease to HIV-specific functions. Memory impairment correlated in real time with hippocampal dysfunction shown by defective long-term potentiation in hippocampal slices
MeSH term(s)	AIDS Dementia Complex/physiopathology ; Animals ; Behavior, Animal ; Cognitive Dysfunction/physiopathology ; Disease Models, Animal ; Hippocampus/pathology ; Hippocampus/virology ; Male ; Memory Disorders/complications ; Memory Disorders/physiopathology ; Mice ; Viral Load
Language	English
Publishing date	2019-07-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.00591-19
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: HIV induces expression of complement component C3 in astrocytes by NF-κB-dependent activation of interleukin-6 synthesis.

Nitkiewicz, Jadwiga / Borjabad, Alejandra / Morgello, Susan / Murray, Jacinta / Chao, Wei / Emdad, Luni / Fisher, Paul B / Potash, Mary Jane / Volsky, David J

Journal of neuroinflammation

2017 Volume 14, Issue 1, Page(s) 23

Abstract: Background: Abnormal activation of the complement system contributes to some central nervous system diseases but the role of complement in HIV-associated neurocognitive disorder (HAND) is unclear.: Methods: We used real-time PCR and ... ...

Abstract	Background: Abnormal activation of the complement system contributes to some central nervous system diseases but the role of complement in HIV-associated neurocognitive disorder (HAND) is unclear. Methods: We used real-time PCR and immunohistochemistry to detect complement expression in postmortem brain tissue from HAND patients and controls. To further investigate the basis for viral induction of gene expression in the brain, we studied the effect of HIV on C3 expression by astrocytes, innate immune effector cells, and targets of HIV. Human fetal astrocytes (HFA) were infected with HIV in culture and cellular pathways and factors involved in signaling to C3 expression were elucidated using pharmacological pathway inhibitors, antisense RNA, promoter mutational analysis, and fluorescence microscopy. Results: We found significantly increased expression of complement components including C3 in brain tissues from patients with HAND and C3 was identified by immunocytochemistry in astrocytes and neurons. Exposure of HFA to HIV in culture-induced C3 promoter activity, mRNA expression, and protein production. Use of pharmacological inhibitors indicated that induction of C3 expression by HIV requires NF-κB and protein kinase signaling. The relevance of NF-κB regulation to C3 induction was confirmed through detection of NF-κB translocation into nuclei and inhibition through overexpression of the physiological NF-κB inhibitor, I-κBα. C3 promoter mutation analysis revealed that the NF-κB and SP binding sites are dispensable for the induction by HIV, while the proximal IL-1β/IL-6 responsive element is essential. HIV-treated HFA secreted IL-6, exogenous IL-6 activated the C3 promoter, and anti-IL-6 antibodies blocked HIV activation of the C3 promoter. The activation of IL-6 transcription by HIV was dependent upon an NF-κB element within the IL-6 promoter. Conclusions: These results suggest that HIV activates C3 expression in primary astrocytes indirectly, through NF-κB-dependent induction of IL-6, which in turn activates the C3 promoter. HIV induction of C3 and IL-6 in astrocytes may contribute to HIV-mediated inflammation in the brain and cognitive dysfunction.
MeSH term(s)	Adult ; Astrocytes/metabolism ; Astrocytes/virology ; Caffeic Acids/pharmacology ; Complement C3/genetics ; Complement C3/metabolism ; Enzyme Activation/drug effects ; Enzyme Activators/pharmacology ; Enzyme Inhibitors/pharmacology ; Female ; Fetus ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/genetics ; Gene Expression Regulation, Viral/physiology ; Glial Fibrillary Acidic Protein/metabolism ; HIV Infections/pathology ; Humans ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Male ; Middle Aged ; NF-kappa B/metabolism ; Phenylethyl Alcohol/analogs & derivatives ; Phenylethyl Alcohol/pharmacology ; Promoter Regions, Genetic/drug effects ; Promoter Regions, Genetic/genetics ; Signal Transduction/drug effects ; Signal Transduction/genetics
Chemical Substances	Caffeic Acids ; Complement C3 ; Enzyme Activators ; Enzyme Inhibitors ; Glial Fibrillary Acidic Protein ; Interleukin-6 ; NF-kappa B ; caffeic acid phenethyl ester (G960R9S5SK) ; Phenylethyl Alcohol (ML9LGA7468)
Language	English
Publishing date	2017-01-26
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-017-0794-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Intranasal insulin therapy reverses hippocampal dendritic injury and cognitive impairment in a model of HIV-associated neurocognitive disorders in EcoHIV-infected mice.

Kim, Boe-Hyun / Kelschenbach, Jennifer / Borjabad, Alejandra / Hadas, Eran / He, Hongxia / Potash, Mary Jane / Nedelcovych, Michael T / Rais, Rana / Haughey, Norman J / McArthur, Justin C / Slusher, Barbara S / Volsky, David J

AIDS (London, England)

2019 Volume 33, Issue 6, Page(s) 973–984

Abstract: Objective: Almost half of HIV-positive people on antiretroviral therapy have demonstrable mild neurocognitive impairment (HIV-NCI), even when virologically suppressed. Intranasal insulin therapy improves cognition in Alzheimer's disease and diabetes. ... ...

Abstract	Objective: Almost half of HIV-positive people on antiretroviral therapy have demonstrable mild neurocognitive impairment (HIV-NCI), even when virologically suppressed. Intranasal insulin therapy improves cognition in Alzheimer's disease and diabetes. Here we tested intranasal insulin therapy in a model of HIV-NCI in EcoHIV-infected conventional mice. Design and methods: Insulin pharmacokinetics following intranasal administration to mice was determined by ELISA. Mice were inoculated with EcoHIV to cause NCI; 23 days or 3 months after infection they were treated daily for 9 days with intranasal insulin (2.4 IU/mouse) and examined for NCI in behavioral tests and HIV burdens by quantitative PCR. Some animals were tested for hippocampal neuronal integrity by immunostaining and expression of neuronal function-related genes by real time-quantitative PCR. The effect of insulin treatment discontinuation on cognition and neuropathology was also examined. Results: Intranasal insulin administration to mice resulted in μIU/ml levels of insulin in cerebrospinal fluid with a half-life of about 2 h, resembling pharmacokinetic parameters of patients receiving 40 IU. Intranasal insulin treatment starting 23 days or 3 months after infection completely reversed NCI in mice. Murine NCI correlated with reductions in hippocampal dendritic arbors and downregulation of neuronal function genes; intranasal insulin reversed these changes coincident with restoration of cognitive acuity, but they returned within 24 h of treatment cessation. Intranasal insulin treatment reduced brain HIV DNA when started 23 but not 90 days after infection. Conclusion: Our preclinical studies support the use of intranasal insulin administration for treatment of HIV-NCI and suggest that some dendritic injury in this condition is reversible.
MeSH term(s)	AIDS Dementia Complex/drug therapy ; Administration, Intranasal ; Animals ; Behavior, Animal ; Cognitive Dysfunction/drug therapy ; Disease Models, Animal ; Hippocampus/pathology ; Hypoglycemic Agents/administration & dosage ; Hypoglycemic Agents/pharmacokinetics ; Immunohistochemistry ; Insulin/administration & dosage ; Insulin/pharmacokinetics ; Mice, Inbred C57BL ; Treatment Outcome ; Viral Load
Chemical Substances	Hypoglycemic Agents ; Insulin
Language	English
Publishing date	2019-04-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639076-6
ISSN	1473-5571 ; 0269-9370 ; 1350-2840
ISSN (online)	1473-5571
ISSN	0269-9370 ; 1350-2840
DOI	10.1097/QAD.0000000000002150
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2228: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Gene expression profiles of HIV-1-infected glia and brain: toward better understanding of the role of astrocytes in HIV-1-associated neurocognitive disorders.

Borjabad, Alejandra / Brooks, Andrew I / Volsky, David J

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2009 Volume 5, Issue 1, Page(s) 44–62

Abstract: Astrocytes are the major cellular component of the central nervous system (CNS), and they play multiple roles in brain development, normal brain function, and CNS responses to pathogens and injury. The functional versatility of astrocytes is linked to ... ...

Abstract	Astrocytes are the major cellular component of the central nervous system (CNS), and they play multiple roles in brain development, normal brain function, and CNS responses to pathogens and injury. The functional versatility of astrocytes is linked to their ability to respond to a wide array of biological stimuli through finely orchestrated changes in cellular gene expression. Dysregulation of gene expression programs, generally by chronic exposure to pathogenic stimuli, may lead to dysfunction of astrocytes and contribute to neuropathogenesis. Here, we review studies that employ functional genomics to characterize the effects of HIV-1 and viral pathogenic proteins on cellular gene expression in astrocytes in vitro. We also present the first microarray analysis of primary mouse astrocytes exposed to HIV-1 in culture. In spite of different experimental conditions and microarray platforms used, comparison of the astrocyte array data sets reveals several common gene-regulatory changes that may underlie responses of these cells to HIV-1 and its proteins. We also compared the transcriptional profiles of astrocytes with those obtained in analyses of brain tissues of patients with HIV-1 dementia and macaques infected with simian immunodeficiency virus (SIV). Notably, many of the gene characteristics of responses to HIV-1 in cultured astrocytes were also altered in HIV-1 or SIV-infected brains. Functional genomics, in conjunction with other approaches, may help clarify the role of astrocytes in HIV-1 neuropathogenesis.
MeSH term(s)	AIDS Dementia Complex/genetics ; Animals ; Astrocytes/metabolism ; Astrocytes/virology ; Brain/cytology ; Brain/metabolism ; Brain/virology ; Gene Expression Profiling/methods ; Genomics/methods ; Human Immunodeficiency Virus Proteins/pharmacology ; Humans
Chemical Substances	Human Immunodeficiency Virus Proteins
Keywords	covid19
Language	English
Publishing date	2009-08-21
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-009-9167-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: EcoHIV infection of mice establishes latent viral reservoirs in T cells and active viral reservoirs in macrophages that are sufficient for induction of neurocognitive impairment.

Gu, Chao-Jiang / Borjabad, Alejandra / Hadas, Eran / Kelschenbach, Jennifer / Kim, Boe-Hyun / Chao, Wei / Arancio, Ottavio / Suh, Jin / Polsky, Bruce / McMillan, JoEllyn / Edagwa, Benson / Gendelman, Howard E / Potash, Mary Jane / Volsky, David J

PLoS pathogens

2018 Volume 14, Issue 6, Page(s) e1007061

Abstract: Suppression of HIV replication by antiretroviral therapy (ART) or host immunity can prevent AIDS but not other HIV-associated conditions including neurocognitive impairment (HIV-NCI). Pathogenesis in HIV-suppressed individuals has been attributed to ... ...

Abstract	Suppression of HIV replication by antiretroviral therapy (ART) or host immunity can prevent AIDS but not other HIV-associated conditions including neurocognitive impairment (HIV-NCI). Pathogenesis in HIV-suppressed individuals has been attributed to reservoirs of latent-inducible virus in resting CD4+ T cells. Macrophages are persistently infected with HIV but their role as HIV reservoirs in vivo has not been fully explored. Here we show that infection of conventional mice with chimeric HIV, EcoHIV, reproduces physiological conditions for development of disease in people on ART including immunocompetence, stable suppression of HIV replication, persistence of integrated, replication-competent HIV in T cells and macrophages, and manifestation of learning and memory deficits in behavioral tests, termed here murine HIV-NCI. EcoHIV established latent reservoirs in CD4+ T lymphocytes in chronically-infected mice but could be induced by epigenetic modulators ex vivo and in mice. In contrast, macrophages expressed EcoHIV constitutively in mice for up to 16 months; murine leukemia virus (MLV), the donor of gp80 envelope in EcoHIV, did not infect macrophages. Both EcoHIV and MLV were found in brain tissue of infected mice but only EcoHIV induced NCI. Murine HIV-NCI was prevented by antiretroviral prophylaxis but once established neither persistent EcoHIV infection in mice nor NCI could be reversed by long-acting antiretroviral therapy. EcoHIV-infected, athymic mice were more permissive to virus replication in macrophages than were wild-type mice, suffered cognitive dysfunction, as well as increased numbers of monocytes and macrophages infiltrating the brain. Our results suggest an important role of HIV expressing macrophages in HIV neuropathogenesis in hosts with suppressed HIV replication.
MeSH term(s)	Adoptive Transfer ; Aged ; Animals ; Anti-Retroviral Agents/therapeutic use ; Brain/virology ; CD4-Positive T-Lymphocytes/virology ; Disease Reservoirs ; Female ; HIV/genetics ; HIV/immunology ; HIV/pathogenicity ; HIV/physiology ; HIV Infections/complications ; HIV Infections/drug therapy ; Humans ; Macrophages, Peritoneal/virology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Middle Aged ; Neurocognitive Disorders/virology ; Plasmids ; Spleen/cytology ; Spleen/immunology
Chemical Substances	Anti-Retroviral Agents
Language	English
Publishing date	2018-06-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1007061
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito