July 1, 1998Journal of VirologyOpen Access

NF-κB-Mediated Inhibition of Apoptosis Is Required for Encephalomyocarditis Virus Virulence: a Mechanism of Resistance in p50 Knockout Mice

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Population

p50 knockout mice, interferon type I receptor knockout mice, double-knockout mice, and murine embryonic…

Comparison

Murine encephalomyocarditis virus (EMCV) infection vs Wild-type mice and normal MEFs infected with EMCV

Design

Preclinical

Authors

ESEdward M. SchwarzSalk Institute for Biological Studies CBCornel BadorffGoethe University Frankfurt THTimothy S. HiuraLos Angeles Medical Center

Discussion

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Implication

Does not inform clinical management of viral myocarditis; leaves open whether p50 inhibition enhances clearance in humans.

Structured PICO

Population

p50 knockout (p50 -/-) mice, interferon type I receptor knockout (IFNRI -/-) mice, double-knockout mice, and murine embryonic fibroblasts (MEF) derived from wild-type, p50 -/-, and p65 -/- embryos

Intervention

Murine encephalomyocarditis virus (EMCV) infection

Comparator

Wild-type mice and normal MEFs infected with EMCV

Outcome

Survival of mice, viral clearance from the heart in vivo, and apoptosis/cytotoxicity in vitro

Suppression of apoptosis by NF-kappaB1 (p50) is required for encephalomyocarditis virus virulence in vivo, and its absence allows rapid apoptosis and viral clearance.

Cite This Study

Schwarz et al. (1998) studied this question.

synapsesocial.com/papers/6a86a2771d4e7816c90cfe98 https://doi.org/10.1128/jvi.72.7.5654-5660.1998

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NF-κB-Mediated Inhibition of Apoptosis Is Required for Encephalomyocarditis Virus Virulence: a Mechanism of Resistance in p50 Knockout Mice

Discussion

Member takes

Implication

Structured PICO

Cite This Study

NF-κB-Mediated Inhibition of Apoptosis Is Required for Encephalomyocarditis Virus Virulence: a Mechanism of Resistance in p50 Knockout Mice

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider