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HIV Neuropathogenesis

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https://www.readbyqxmd.com/read/29705605/the-role-of-catecholamines-in-hiv-neuropathogenesis
#1
R Nolan, P J Gaskill
The success of anti-retroviral therapy has improved the quality of life and lifespan of HIV+ individuals, transforming HIV infection into a chronic condition. These improvements have come with a cost, as chronic HIV infection and long-term therapy have resulted in the emergence of a number of new pathologies. This includes a variety of the neuropathological and neurocognitive effects collectively known as HIVassociated neurocognitive disorders (HAND) or NeuroHIV. These effects persist even in the absence of viral replication, suggesting that they are mediated the long-term changes in the CNS induced by HIV infection rather than by active replication...
April 26, 2018: Brain Research
https://www.readbyqxmd.com/read/29703241/human-immunodeficiency-virus-type-1-hiv-1-mediated-neuroinflammation-dysregulates-neurogranin-and-induces-synaptodendritic-injury
#2
Debjani Guha, Marc C E Wagner, Velpandi Ayyavoo
BACKGROUND: Human immunodeficiency virus type 1 (HIV-1)-associated neurocognitive disorder (HAND) is a common outcome of a majority of HIV-1-infected subjects and is associated with synaptodendritic damage. Neurogranin (Ng), a postsynaptic protein, and calmodulin (CaM) are two important players of synaptic integrity/functions. The biological role of Ng in the context of HAND is unknown. METHODS: We compared the expression of Ng in frontal cortex (FC) tissues from control and HIV-1-positive subjects with and without HAND by immunohistochemistry, western blot, and qRT-PCR...
April 27, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29698322/lentiviral-infection-of-proliferating-brain-macrophages-in-hiv-and-simian-immunodeficiency-virus-encephalitis-despite-sterile-alpha-motif-and-histidine-aspartate-domain-containing-protein-1-expression
#3
Allison A Lindgren, Adam R Filipowicz, Julian B Hattler, Soon Ok Kim, Hye Kyung Chung, Marcelo J Kuroda, Edward M Johnson, Woong-Ki Kim
OBJECTIVE: HIV-1 infection of the brain and related cognitive impairment remain prevalent in HIV-1-infected individuals despite combination antiretroviral therapy. Sterile alpha motif and histidine-aspartate domain-containing protein 1 (SAMHD1) is a newly identified host restriction factor that blocks the replication of HIV-1 and other retroviruses in myeloid cells. Cell cycle-regulated phosphorylation at residue Thr592 and viral protein X (Vpx)-mediated degradation of SAMHD1 have been shown to bypass SAMHD1 restriction in vitro...
May 15, 2018: AIDS
https://www.readbyqxmd.com/read/29670623/human-immune-system-mice-for-the-study-of-human-immunodeficiency-virus-type-1-infection-of-the-central-nervous-system
#4
REVIEW
Teresa H Evering, Moriya Tsuji
Immunodeficient mice transplanted with human cell populations or tissues, also known as human immune system (HIS) mice, have emerged as an important and versatile tool for the in vivo study of human immunodeficiency virus-type 1 (HIV-1) pathogenesis, treatment, and persistence in various biological compartments. Recent work in HIS mice has demonstrated their ability to recapitulate critical aspects of human immune responses to HIV-1 infection, and such studies have informed our knowledge of HIV-1 persistence and latency in the context of combination antiretroviral therapy...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29604983/animal-models-of-hiv-associated-disease-of-the-central-nervous-system
#5
Jaclyn Mallard, Kenneth C Williams
It is difficult to study the pathogenesis of human immunodeficiency virus (HIV)-associated neurocognitive disorder (HAND) in living patients because central nervous system (CNS) tissues are only available post mortem. Rodent and nonhuman primate (NHP) models of HAND allow for longitudinal analysis of HIV-associated CNS pathology and efficacy studies of novel therapeutics. Rodent models of HAND allow for studies with large sample sizes, short duration, and relatively low cost. These models include humanized mice used to study HIV-associated neuropathogenesis and transgenic mice used to study neurotoxic effects of viral proteins without infection...
2018: Handbook of Clinical Neurology
https://www.readbyqxmd.com/read/29604978/neuropathogenesis-of-human-immunodeficiency-virus-infection
#6
Brady Sillman, Christopher Woldstad, Joellyn Mcmillan, Howard E Gendelman
Human immunodeficiency virus (HIV)-associated neurocognitive disorders (HAND) remain a common end-organ manifestation of viral infection. Subclinical and mild symptoms lead to neurocognitive and behavioral abnormalities. These are associated, in part, with viral penetrance and persistence in the central nervous system. Infections of peripheral blood monocytes, macrophages, and microglia are the primary drivers of neuroinflammation and neuronal impairments. While current antiretroviral therapy (ART) has reduced the incidence of HIV-associated dementia, milder forms of HAND continue...
2018: Handbook of Clinical Neurology
https://www.readbyqxmd.com/read/29549313/astrocytic-metabolic-switch-is-a-novel-etiology-for-cocaine-and-hiv-1-tat-mediated-neurotoxicity
#7
Kalimuthusamy Natarajaseenivasan, Bianca Cotto, Santhanam Shanmughapriya, Alyssa A Lombardi, Prasun K Datta, Muniswamy Madesh, John W Elrod, Kamel Khalili, Dianne Langford
Calcium (Ca2+ ) dynamics and oxidative signaling control mitochondrial bioenergetics in the central nervous system, where astrocytes are a major energy source for neurons. Cocaine use exacerbates HIV-associated neurocognitive disorders, but little is known about disruptions in astrocyte metabolism in this context. Our data show that the HIV protein Tat and cocaine induce a metabolic switch from glucose to fatty acid oxidation in astrocytes, thereby limiting lactate transport to neurons. Mechanistic analyses revealed increased Mitochondrial Ca2+ Uniporter (MCU)-mediated Ca2+ uptake in astrocytes exposed to Tat and cocaine due to oxidation of MCU...
March 16, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29547435/lentiviral-infection-of-proliferating-brain-macrophages-in-siv-and-hiv-encephalitis-despite-samhd1-expression
#8
Allison A Lindgren, Adam R Filipowicz, Julian B Hattler, Soon Ok Kim, Hye Kyung Chung, Marcelo J Kuroda, Edward M Johnson, Woong-Ki Kim
OBJECTIVE: HIV-1 infection of the brain and related cognitive impairment remain prevalent in HIV-1-infected subjects despite combination antiretroviral therapy. Sterile alpha motif and histidine-aspartate domain-containing protein 1 (SAMHD1) is a newly identified host restriction factor that blocks the replication of HIV-1 and other retroviruses in myeloid cells. Cell-cycle-regulated phosphorylation at residue Thr592 and viral protein X (Vpx)-mediated degradation of SAMHD1 have been shown to bypass SAMHD1 restriction in vitro...
March 15, 2018: AIDS
https://www.readbyqxmd.com/read/29510721/heme-oxygenase-1-promoter-region-gt-n-polymorphism-associates-with-increased-neuroimmune-activation-and-risk-for-encephalitis-in-hiv-infection
#9
Alexander J Gill, Rolando Garza, Surendra S Ambegaokar, Benjamin B Gelman, Dennis L Kolson
BACKGROUND: Heme oxygenase-1 (HO-1) is a critical cytoprotective enzyme that limits oxidative stress, inflammation, and cellular injury within the central nervous system (CNS) and other tissues. We previously demonstrated that HO-1 protein expression is decreased within the brains of HIV+ subjects and that this HO-1 reduction correlates with CNS immune activation and neurocognitive dysfunction. To define a potential CNS protective role for HO-1 against HIV, we analyzed a well-characterized HIV autopsy cohort for two common HO-1 promoter region polymorphisms that are implicated in regulating HO-1 promoter transcriptional activity, a (GT)n dinucleotide repeat polymorphism and a single nucleotide polymorphism (A(-413)T)...
March 6, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29497921/exosomal-mir-9-released-from-hiv-tat-stimulated-astrocytes-mediates-microglial-migration
#10
Lu Yang, Fang Niu, Honghong Yao, Ke Liao, Xufeng Chen, Yeonhee Kook, Rong Ma, Guoku Hu, Shilpa Buch
Chronic neuroinflammation still remains a common underlying feature of HIV-infected patients on combined anti-retroviral therapy (cART). Previous studies have reported that despite near complete suppression of virus replication by cART, cytotoxic viral proteins such as HIV trans-activating regulatory protein (Tat) continue to persist in tissues such as the brain and the lymph nodes, thereby contributing, in part, to chronic glial activation observed in HIV-associated neurological disorders (HAND). Understanding how the glial cells cross talk to mediate neuropathology is thus of paramount importance...
March 1, 2018: Journal of Neuroimmune Pharmacology: the Official Journal of the Society on NeuroImmune Pharmacology
https://www.readbyqxmd.com/read/29467577/human-immunodeficiency-virus-in-the-brain-culprit-or-facilitator
#11
REVIEW
Luminita Ene
Introduction: Human immunodeficiency virus (HIV) enters the brain early, where it can persist, evolve, and become compartmentalized. Central nervous system (CNS) disease can be attributed to HIV alone or to the complex interplay between the virus and other neurotropic pathogens. Aim: The current review aims to describe the direct impact of HIV on the brain as well as its relationship with other pathogens from a practitioner's perspective, to provide a general clinical overview, brief workup, and, whenever possible, treatment guidance...
2018: Infectious Diseases
https://www.readbyqxmd.com/read/29369399/expression-profiling-suggests-microglial-impairment-in-human-immunodeficiency-virus-neuropathogenesis
#12
Stephen D Ginsberg, Melissa J Alldred, Satya M Gunnam, Consuelo Schiroli, Sang Han Lee, Susan Morgello, Tracy Fischer
OBJECTIVE: CD16+ /CD163+ macrophages (MΦs) and microglia accumulate in the brains of patients with human immunodeficiency virus (HIV) encephalitis (HIVE), a neuropathological correlate of the most severe form of HIV-associated neurocognitive disorders, HIV-associated dementia. Recently, we found that some parenchymal microglia in brain of HIV+ subjects without encephalitis (HIV/noE) but with varying degrees of neurocognitive impairment express CD16 and CD163, even in the absence of detectable virus production...
February 2018: Annals of Neurology
https://www.readbyqxmd.com/read/29259541/connexin43-containing-gap-junction-channels-facilitate-hiv-bystander-toxicity-implications-in-neurohiv
#13
Shaily Malik, Martin Theis, Eliseo A Eugenin
Human immunodeficiency virus-1 (HIV-1) infection compromises the central nervous system (CNS) in a significant number of infected individuals, resulting in neurological dysfunction that ranges from minor cognitive deficits to frank dementia. While macrophages/microglia are the predominant CNS cells infected by HIV, our laboratory and others have shown that HIV-infected astrocytes, although present in relatively low numbers with minimal to undetectable viral replication, play key role in NeuroAIDS pathogenesis...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29247305/neurologic-disease-in-feline-immunodeficiency-virus-infection-disease-mechanisms-and-therapeutic-interventions-for-neuroaids
#14
Christopher Power
Feline immunodeficiency virus (FIV) is a lentivirus that causes immunosuppression through virus-mediated CD4+ T cell depletion in feline species. FIV infection is complicated by virus-induced disease in the nervous system. FIV enters the brain soon after primary infection and is detected as FIV-encoded RNA, DNA, and proteins in microglia, macrophages, and astrocytes. FIV infection activates neuroinflammatory pathways including cytokines, chemokines, proteases, and ROS with accompanying neuronal injury and loss...
December 15, 2017: Journal of Neurovirology
https://www.readbyqxmd.com/read/29235371/hybrid-2d-3d-quantitative-structure-activity-relationship-and-modeling-studies-perspectives-of-pepstatin-a-analogs-as-cathepsin-d-inhibitors
#15
Olayide A Arodola, Mahmoud Es Soliman
AIM: Cathepsin D, one of the attractive targets in the treatment of breast cancer, has been implicated in HIV neuropathogenesis with potential proteolytic effects on chemokines. Methodology/result: Diverse modeling tools were used to reveal the key structural features affecting the inhibitory activities of 78 pepstatin A analogs. Analyses were performed to investigate the stability, rationality and fluctuation of the analogs. Results showed a clear correlation between the experimental and predicted activities of the analogs as well as the variation in their activities relative to structural modifications...
January 2018: Future Medicinal Chemistry
https://www.readbyqxmd.com/read/29128906/toll-like-receptor-3-mediates-hiv-1-induced-interleukin-6-expression-in-the-human-brain-endothelium-via-tak1-and-jnk-pathways-implications-for-viral-neuropathogenesis
#16
Biju Bhargavan, Georgette D Kanmogne
HIV-1-associated neurocognitive disorders (HAND) is associated with blood-brain-barrier (BBB) inflammation, and inflammation involves toll-like receptors (TLRs) signaling. It is not known whether primary human brain microvascular endothelial cells (HBMEC), the major BBB component, express TLRs or whether TLRs are involved in BBB dysfunction and HAND. We demonstrate that HBMEC express TLR3, 4, 5, 7, 9, and 10, and TLR3 was the most abundant. HIV-1 and TLR3 activation increased endothelial TLR3 transcription and expression...
November 11, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/29058550/immunomodulatory-role-of-complement-proteins-in-the-neuropathology-associated-with-opiate-abuse-and-hiv-1-co-morbidity
#17
Supriya D Mahajan, Ravikumar Aalinkeel, Neil U Parikh, Alexander Jacob, Katherine Cwiklinski, Prateet Sandhu, Kevin Le, Alexander W Loftus, Stanley A Schwartz, Richard J Quigg, Jessy J Alexander
The complement system which is a critical mediator of innate immunity plays diverse roles in the neuropathogenesis of HIV-1 infection such as clearing HIV-1 and promoting productive HIV-1 replication. In the development of HIV-1 associated neurological disorders (HAND), there may be an imbalance between complement activation and regulation, which may contribute to the neuronal damage as a consequence of HIV-1 infection. It is well recognized that opiate abuse exacerbates HIV-1 neuropathology, however, little is known about the role of complement proteins in opiate induced neuromodulation, specifically in the presence of co-morbidity such as HIV-1 infection...
November 2017: Immunological Investigations
https://www.readbyqxmd.com/read/29056673/feline-immunodeficiency-virus-neuropathogenesis-a-model-for-hiv-induced-cns-inflammation-and-neurodegeneration
#18
REVIEW
Rick B Meeker, Lola Hudson
Feline Immunodeficiency virus (FIV), similar to its human analog human immunodeficiency virus (HIV), enters the central nervous system (CNS) soon after infection and establishes a protected viral reservoir. The ensuing inflammation and damage give rise to varying degrees of cognitive decline collectively known as HIV-associated neurocognitive disorders (HAND). Because of the similarities to HIV infection and disease, FIV has provided a useful model for both in vitro and in vivo studies of CNS infection, inflammation and pathology...
March 6, 2017: Veterinary Sciences
https://www.readbyqxmd.com/read/28978127/hiv-1-gp120-clade-b-c-induces-a-grp78-driven-cytoprotective-mechanism-in-astrocytoma
#19
Sheila N López, Madeline Rodríguez-Valentín, Mariela Rivera, Maridaliz Rodríguez, Mohan Babu, Luis A Cubano, Huangui Xiong, Guangdi Wang, Lilia Kucheryavykh, Nawal M Boukli
HIV-1 clades are known to be one of the key factors implicated in modulating HIV-associated neurocognitive disorders. HIV-1 B and C clades account for the majority of HIV-1 infections, clade B being the most neuropathogenic. The mechanisms behind HIV-mediated neuropathogenesis remain the subject of active research. We hypothesized that HIV-1 gp120 clade B and C proteins may exert differential proliferation, cell survival and NeuroAIDS effects in human astrocytoma cells via the Unfolded Protein Response, an endoplasmic reticulum- based cytoprotective mechanism...
September 15, 2017: Oncotarget
https://www.readbyqxmd.com/read/28975505/an-siv-macaque-model-targeted-to-study-hiv-associated-neurocognitive-disorders
#20
REVIEW
Sarah E Beck, Suzanne E Queen, Kelly A Metcalf Pate, Lisa M Mangus, Celina M Abreu, Lucio Gama, Kenneth W Witwer, Robert J Adams, M Christine Zink, Janice E Clements, Joseph L Mankowski
Simian immunodeficiency virus (SIV) infection of pigtailed macaques is a highly representative and well-characterized animal model for HIV neuropathogenesis studies that provides an excellent opportunity to study and develop prognostic markers of HIV-associated neurocognitive disorders (HAND) for HIV-infected individuals. SIV studies can be performed in a controlled setting that enhances reproducibility and offers high-translational value. Similar to observations in HIV-infected patients receiving antiretroviral therapy (ART), ongoing neurodegeneration and inflammation are present in SIV-infected pigtailed macaques treated with suppressive ART...
October 3, 2017: Journal of Neurovirology
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