Related Experiment Video
Updated: Jul 19, 2026

08:32
Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Mouse hepatitis virus does not induce Beta interferon synthesis and does not inhibit its induction by double-stranded
1Department of Microbiology, University of Iowa, Bowen Science Building 3-730, Iowa City, IA 52242, USA.
Journal of Virology
|November 3, 2006
Summary
Mouse hepatitis virus (MHV) evades interferon production by preventing key transcription factor activation. This evasion is not due to direct inhibition of cellular antiviral responses to other stimuli.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Mouse hepatitis virus (MHV) is known to evade host immune responses.
- Interferon (IFN) production is a critical antiviral defense mechanism.
- Fibroblasts and dendritic cells are key players in innate immunity against viral infections.
Purpose of the Study:
- To investigate the mechanism by which MHV evades interferon production.
- To determine if MHV interferes with essential interferon transcription factors.
- To assess MHV's impact on pattern recognition receptor (PRR) signaling pathways.
Main Methods:
- Infection of fibroblasts and bone marrow-derived dendritic cells with MHV.
- Analysis of nuclear translocation and activation of NF-kappaB and IFN regulatory factor 3.
- Stimulation with poly(I:C) to assess response inhibition.
- Evaluation of IFN-beta production mediated by RIG-I, Mda-5, and TLR3.
Main Results:
- MHV infection did not induce interferon production in tested cells.
- Essential IFN-beta transcription factors (NF-kappaB, IFN regulatory factor 3) were not activated during MHV infection.
- MHV did not inhibit IFN-beta production induced by poly(I:C) or mediated by known PRRs.
- These findings suggest viral double-stranded RNA is inaccessible to cellular PRRs.
Conclusions:
- MHV employs a mechanism to evade interferon induction that does not involve direct inhibition of cellular antiviral signaling.
- The inaccessibility of viral double-stranded RNA to cellular pattern recognition receptors is a likely cause of immune evasion.
Related Concept Videos
Inhibitors of Viral Protein Synthesis
Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Hepatitis
Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Viruses with RNA Genomes
RNA viruses are categorized into positive-strand, negative-strand, or double-stranded groups based on their genomic structure and replication mechanisms. This classification dictates how they exploit host cellular machinery for protein synthesis and replication. Some RNA viruses also utilize reverse transcription as part of their life cycle, further diversifying their replication strategies.Positive-Strand RNA VirusesPositive-strand RNA viruses have genomes that function directly as messenger...
Inhibitors Of Virion Release
Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
Viral Hepatitis I: Introduction
Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
Inhibitors of Virion Maturation and Assembly
As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...

