Related Experiment Video
Updated: May 7, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Cardioselective infection with coxsackievirus B3 requires intact type I interferon signaling: implications for
R Wessely1, K Klingel, K U Knowlton
1Deutsches Herzzentrum and 1 Medizinische Klinik, Technische Universität, Munich, Germany.
Background:
Interferons (IFNs) play an important role in antiviral defense and have therapeutic potential in coxsackievirus heart disease. However, little is known about the relative contributions of type I and type II IFN signaling in coxsackievirus B3 (CVB3) infection or their role in the cardioselective nature of CVB3 infection.
Methods And Results:
Wild-type mice and mice deficient for either the type I or the type II IFN receptor (IFNR) were infected with CVB3. Infection of the type I IFNR-deficient mice with >10(3) plaque-forming units (pfu) of CVB3 resulted in 100% mortality within 2 to 4 days after infection. Death was rare in wild-type and type II IFNR-deficient mice after inoculation with as much as 10(8) pfu of CVB3. Surprisingly, the early mortality in the type I IFNR-deficient mice was not accompanied by higher virus titers in the heart. Unexpectedly, a dramatic increase of viral RNA in the liver was found to correlate with early mortality in type I IFNR-deficient mice.
Conclusions:
Type I but not type II IFN signaling is essential for the prevention of early death due to CVB3 infection. Interestingly, neither type I or type II IFN signaling has a dramatic effect on early viral replication in the heart. However, lethal viral replication in the liver is controlled by type I IFNs. These results demonstrate that the IFN system is capable of modulating both viral pathogenicity and tissue tropism.
More Related Videos
Related Concept Videos
Endocarditis I: Introduction
Endocarditis II: Clinical Features of Infective Endocarditis
Endocarditis III: Medical Management
Myocarditis III: Medical Management
Cytomegalovirus Disease
Inhibitors of Viral Protein Synthesis

