Virus-induced Transcriptional Suppression
Virus-induced Transcriptional Suppression - Related Videos
03:35
Analysis of Virus-Induced Host Transcriptional Suppression Using Flow Cytometry
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2026
Source: Kalveram, B., et al. Using Click Chemistry to Measure the Effect of Viral Infection on Host-Cell RNA Synthesis. J. Vis. Exp. (2013)This video demonstrates the use of click chemistry and flow cytometry to measure virus-induced suppression of host-cell transcription. Mammalian cells are infected with a virus that expresses a nuclear virulence protein disrupting the host transcription factor complex, while control cells remain transcriptionally active. Incorporation of 5-ethynyl uridine...
04:29
Visualizing Transcriptional Suppression in Virus-Infected Cells
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2026
Source: Kalveram, B. et al. Using Click Chemistry to Measure the Effect of Viral Infection on Host-Cell RNA Synthesis. J. Vis. Exp. (2013)This video demonstrates the use of click chemistry and fluorescence microscopy to visualize nascent RNA transcription in mammalian cells. It highlights how viral infection suppresses host transcription by comparing fluorescent signals between infected and control cells.
03:08
Production of Reporter-Containing Ebola Virus Transcription- and Replication-Competent Virus-Like Particles
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2026
Source: Hoenen, T., et al. Modeling The Lifecycle Of Ebola Virus Under Biosafety Level 2 Conditions With Virus-like Particles Containing Tetracistronic Minigenomes. J. Vis. Exp. (2014)This video demonstrates how a tetracistronic minigenome plasmid mimicking the Ebola virus genome is transfected into human cells along with helper plasmids. Inside the cells, viral proteins and luciferase are expressed, leading to the assembly and budding of non-pathogenic, replication-competent virus-like...
02:50
Suppressing Hepatitis B Virus Replication Using Viral Antigen-Specific T Cells
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2025
The video demonstrates an assay using human induced pluripotent stem cell (iPSC)-derived CD8+ T cells to inhibit hepatitis B virus (HBV) replication in mice. These T cells, engineered with HBV-specific receptors, are transferred into transgenic mice. Replication-competent HBV genome plasmids are then injected directly into the liver, enabling viral DNA uptake. Once viral antigens are expressed and presented by hybrid MHC-I molecules, the engineered T cells recognize and bind to these complexes.
11:00
Reprogramming Mouse Embryonic Fibroblasts with Transcription Factors to Induce a Hemogenic Program
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Cited by 1 •
2016
The protocol described here details the induction of a hemogenic program in mouse embryonic fibroblasts via overexpression of a minimal set of transcription factors. This technology may be translated to the human system to provide platforms for future study of hematopoiesis, hematologic disease, and hematopoietic stem cell transplant.
FAQs
Viral infection may act at several control points rather than through a single mechanism. It can disrupt transcription factors, alter signaling pathways, interfere with chromatin regulation, or affect RNA polymerase II activity. Because these components coordinate gene activation, their disruption can reduce transcription across groups of host genes and produce broad changes in infected-cell function.
Reducing transcription of antiviral genes can weaken the host cell’s response during infection. At the same time, limiting expression of other host genes may alter normal cellular activities and help redirect cellular resources toward viral replication. This combination supports immune evasion and can make the intracellular environment more favorable for continued infection.
Four major control systems provide useful points of analysis: transcription factors, signaling pathways, chromatin regulation, and RNA polymerase II. Each can influence whether host genes are transcribed, so disruption at any one of these levels may contribute to reduced gene expression. Examining them helps connect molecular changes with altered infected-cell behavior.
The process illustrates how viral replication and host-cell regulation are interconnected. Viral effects on transcription can change immune responses, cellular behavior, and access to resources, while the host’s regulatory systems influence the course of infection. Studying these reciprocal effects places transcriptional suppression within the broader biology of host-pathogen interactions rather than treating it as an isolated event.
Experimental analysis can focus on whether infection changes host gene transcription and which regulatory components are affected. Investigators can examine the involvement of transcription factors, signaling pathways, chromatin regulation, or RNA polymerase II, then relate those changes to antiviral gene expression and infected-cell behavior. These comparisons help identify potential host or viral factors driving the response.
Virus-induced transcriptional suppression connects molecular regulation with immune evasion and disease development. Identifying the host or viral factors responsible for disrupted transcription may reveal targets for antiviral therapies. The same analysis can clarify how infected cells change their behavior, providing biological context for understanding disease-related effects without focusing only on viral replication itself.