Plaque Burden
Plaque Burden - Related Videos
13:00
Plaque Assay: A Method to Determine Viral Titer as Plaque Forming Units (PFU)
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2023
Source: Tilde Andersson1, Rolf Lood1 1 Department of Clinical Sciences Lund, Division of Infection Medicine, Biomedical Center, Lund University, 221 00 Lund, Sweden Viruses that infect prokaryotic organisms, called bacteriophages or simply phages, were identified in the early 20th century by Twort (1) and d'Hérelle (2) independently. Phages have since been widely recognized for their therapeutic value (3) and their influence on human (4), as well as global, ecosystems (5). Current concerns have...
10:53
Plaque Assay for Murine Norovirus
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Cited by 99 •
2012
Here we describe a method to quantify infectious particles of murine norovirus (MNV), which is the only norovirus that efficiently replicates in cell culture. The plaque assay takes advantage of MNV’s tropism for murine macrophages and can be adapted for use with biological or environmental samples containing MNV.
03:25
Quantification of Pseudovirus Particles by Plaque Assay
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2026
Source: Jamieson, T. R., et al., Detection of SARS-CoV-2 Neutralizing Antibodies using High-Throughput Fluorescent Imaging of Pseudovirus Infection. J. Vis. Exp. (2021)This video describes the virus plaque assay using coronavirus pseudovirus particles. The diluted pseudovirus is added to a monolayer of mammalian cells, followed by incubation with a methylcellulose overlay. Plaques formed by infected cells are counted visually to determine the infectious virus titer.
02:03
Assessing Bacterial Burden in the Mouse Spleen for Infection Studies
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2026
Source: Madenspacher, J. H. and Fessler, M. B. A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice. J. Vis. Exp. (2016)This video demonstrates the process of quantifying bacterial load in the spleen of an infected mouse to assess the severity of infection. The homogenized spleen is serially diluted and plated to determine total bacterial burden. The resulting data provide insights into host-pathogen interactions within...
03:30
Assessing Rotavirus Growth Curve by Plaque Assay
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2026
Source: Kadoya, S., Sano, D. Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus. J. Vis. Exp. (2019).This video demonstrates the use of a plaque assay to assess the rotavirus growth curve. The method involves infecting host cells with diluted virus, overlaying with agarose to restrict spread, and staining to visualize plaques formed by viral replication. By counting plaque-forming units at defined time points, the resulting growth curve reveals the lag, exponential, and...
FAQs
Retained lipids can activate the endothelium, the vessel lining, and promote recruitment of immune cells into the arterial wall. Macrophages then ingest the lipids and become foam cells. This sequence links an initiating lipid-retention event with cellular accumulation, helping explain how lesions develop rather than simply enlarge as inert deposits.
Lesion growth reflects more than lipid accumulation alone. Extracellular matrix, which provides structural material outside cells, and cellular debris also add to the expanding lesion. Together with foam-cell formation, these components influence the tissue’s composition, so two lesions with similar dimensions may still differ biologically in ways relevant to disease assessment.
Size and distribution describe different aspects of disease extent. Size indicates how much tissue is occupied by a lesion, whereas distribution shows where accumulation occurs within the tissue or along blood vessels. Recording both can reveal whether disease is localized or more widespread, giving a fuller interpretation than a single measurement of lesion extent.
Researchers assess plaque burden through imaging, histological analysis, or molecular assays. Imaging supports evaluation within vascular tissue, histology provides a tissue-based analysis, and molecular assays add molecular measurements. Selecting or combining these approaches allows investigators to quantify disease extent while examining lesions at complementary levels of biological organization.
Comparing plaque burden measurements across experiments can show whether disease extent changes during progression or after an experimental treatment. The resulting data support assessment of treatment effects and lesion development rather than relying only on descriptive observations. Consistent measurement also helps relate biological changes in lesions to broader evaluations of vascular risk.
Measuring composition alongside plaque size is especially useful when lesions must be distinguished by likely stability. A size measurement alone describes extent, but composition can clarify differences between more stable lesions and those more likely to rupture. This combined interpretation connects structural observations with the biological features that matter for vascular risk.