Hiv Viral Reservoirs
Hiv Viral Reservoirs - Related Videos
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.
05:46
Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
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Cited by 15 •
2014
Here we describe cellular cytotoxicity and single round infectivity assays that allow for the rapid and accurate screening of compounds to determine their cellular cytotoxicity (CC50) and IC50 values against WT and drug resistant HIV-1.
14:40
Exploring m6A and m5C Epitranscriptomes upon Viral Infection: an Example with HIV
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Cited by 2 •
2022
The role of RNA modifications in viral infections is just starting to be explored and could highlight new viral-host interaction mechanisms. In this work, we provide a pipeline to investigate m6A and m5C RNA modifications in the context of viral infections.
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.
13:08
Visualizing Cell-to-cell Transfer of HIV using Fluorescent Clones of HIV and Live Confocal Microscopy
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Cited by 4 •
2010
This visualized experiment is a guide for utilizing a fluorescent molecular clone of HIV for live confocal imaging experiments.
FAQs
Integration into the host genome gives HIV a durable genetic form that can persist inside a cell even when active viral production is limited. In a resting or long-lived cell, this provirus may remain latent, so immune clearance has little active viral target to recognize. This genomic persistence explains why treatment can suppress infection without removing every source capable of renewed replication.
Antiretroviral therapy acts mainly on active steps of viral replication, whereas a silent provirus in a reservoir cell is largely unaffected by those drugs. The distinction is mechanistically important: medication can prevent new rounds of infection while latent infected cells remain. Reservoir research therefore focuses on both maintaining suppression and addressing persistence at the cellular level.
In the central nervous system, microglia and macrophages can serve as cellular niches for persistent infection. Their location behind the blood-brain barrier may limit access by circulating immune factors and complicate intervention. Studying these cells helps connect reservoir persistence with neuroinflammation and cognitive effects, while emphasizing that any cure strategy must protect neural tissue.
Cellular state is a major determinant of reservoir behavior. Resting cells can maintain integrated HIV DNA with little evidence of active production, while latency-reversal conditions may expose infected cells to immune recognition. This creates a central tradeoff for cure research: activating a reservoir may improve visibility, but the response must be controlled so it does not injure surrounding neural tissue.
Molecular detection and anatomical mapping provide complementary information. Molecular detection can identify HIV-related genetic material in sampled cells, while anatomical mapping shows where infected cell populations are located. In neuroscience, combining these approaches helps distinguish cellular and regional patterns in the central nervous system and relate them to neuroinflammation or cognitive effects.
Latency-reversal approaches are intended to make silent infection more detectable, whereas immune-based approaches aim to help eliminate or control infected cells. Neuroscience studies must assess these strategies in the context of the brain, where excessive activation or immune injury could damage neural tissue. Their value depends on reducing reservoir persistence while preserving neurological function.
Findings from reservoir studies can link the presence and location of persistent infected cells with downstream brain effects. That connection helps researchers evaluate whether a candidate strategy addresses biological sources of neuroinflammation rather than merely suppressing infection. The broader application is to inform durable-remission strategies that address CNS persistence while minimizing harm to neural tissue.