Hiv-1 Encephalitic Mice
Hiv-1 Encephalitic Mice - Related Videos
10:49
In vitro Uncoating of HIV-1 Cores
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Cited by 47 •
2011
Uncoating is an essential step in the early phase of the HIV-1 life cycle and is defined as the disassembly of the capsid shell and the release of the viral ribonucleoprotein complex (vRNP). Here, we demonstrate techniques for isolating intact cores from HIV-1 virions and for quantifying their uncoating in vitro.
13:58
Amplifying and Quantifying HIV-1 RNA in HIV Infected Individuals with Viral Loads Below the Limit of Detection by Standard Clinical Assays
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Cited by 10 •
2011
Quantifying levels of HIV-1 RNA in plasma and sequencing single HIV-1 genomes from individuals with viral loads below the limit of detection (50-75 copies/ml) is difficult. Here we describe how to extract and quantify plasma viral RNA using a real time PCR assay that reliably measures HIV-1 RNA down to 0.3 copies/ml and how to amplify viral genomes by single genome sequencing, from samples with very low viral loads.
10:12
Measuring Endoplasmic Reticulum Stress and Unfolded Protein Response in HIV-1 Infected T-Cells and Analyzing its Role in HIV-1 Replication
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Cited by 1 •
2024
Here, we describe some established methods to determine endoplasmic reticulum (ER) stress and unfolded protein response (UPR) activation, with particular emphasis on HIV-1 infection. This article also describes a set of protocols to investigate the effect of ER stress/UPR on HIV-1 replication and virion infectivity.
06:46
Isolation of Exosomes from the Plasma of HIV-1 Positive Individuals
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Cited by 51 •
2016
Techniques describing a gradient procedure to separate exosomes from human immunodeficiency virus (HIV) particles are described. This procedure was used to isolate exosomes away from HIV particles in human plasma from HIV-infected individuals. The isolated exosomes were analyzed for cytokine/chemokine content.
09:27
New Tools to Expand Regulatory T Cells from HIV-1-infected Individuals
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Cited by 4 •
2013
CD4+ Regulatory T cells are potent immune-modulators and serve important functions in immune homeostasis. The paucity of these cells in peripheral blood makes functional studies challenging, specifically in the context of HIV-1-infection. We here describe a method to isolate and expand functional CD4+ Tregs from peripheral blood from HIV-1-infected individuals.
FAQs
Human HIV-1-infected macrophages or other human immune components act as the initiating source of infection-related signaling within the mouse brain environment. Their presence can provoke neuroinflammation and encephalitic lesions, creating measurable consequences of viral neuropathogenesis. This mechanism allows investigators to examine how infected immune cells interact with neural tissues even though ordinary murine cells are generally not permissive to HIV-1.
Immunodeficient mice provide a host environment in which introduced human immune components can be established for experimental study. That feature is central because standard mouse biology does not naturally support the relevant HIV-1 infection process. By combining the mouse platform with human infected cells, researchers can investigate immune-cell interactions and their relationship to inflammation and tissue injury under controlled conditions.
Neuroinflammation and encephalitic lesions are key outcomes because they indicate how introduced HIV-1-infected cells affect the brain. These findings help connect cellular interactions with broader patterns of HIV-1 neuropathogenesis. Examining such outcomes also gives bioengineering studies a way to evaluate whether an engineered tissue, delivery system, or neuroprotective intervention changes the extent of HIV-1-related neurological injury.
A general workflow begins with an immunodeficient mouse platform, followed by introduction of human HIV-1-infected macrophages or other human immune components. The resulting model is then examined for neuroinflammation and encephalitic lesions. This sequence links model construction to disease-relevant outcomes while preserving experimental control over the human cellular component used to study viral neuropathogenesis.
Bioengineers can use these models as testing platforms for engineered tissues, drug-delivery systems, and neuroprotective interventions aimed at HIV-1-related neurological injury. The model supplies disease-relevant inflammation and lesions against which an intervention can be assessed. Its controlled design supports comparison of how a candidate strategy affects immune-cell interactions, brain inflammation, or tissue damage in a living system.
Their value comes from combining the physiological setting of a mouse with human cellular components that support study of HIV-1-associated brain pathology. Standard mice alone cannot reproduce the relevant disease process because murine cells are generally not permissive to HIV-1. Consequently, the engineered or engrafted model expands experimental access to viral neuropathogenesis, therapeutic testing, and bioengineering research.