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March 1, 2003Journal of Interferon & Cytokine Research

Loss of Stat1 in adult mice resulted in up to 100-fold more rotavirus shedding compared to wild-type mice, but did not impair viral clearance or protection against subsequent challenge.

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Population

Stat1 knock-out mice (Stat1(-/-)) and immunocompetent wild-type (WT) control mice (suckling and adult)

Comparison

Oral infection with rotavirus or vaccination… vs Immunocompetent (WT) mice or unimmunized controls

Design

Preclinical

Follow-up

2-6 days after infection

Key result

Loss of Stat1 in adult mice resulted in up to 100-fold more rotavirus shedding compared to wild-type mice, but did not impair viral clearance or protection against subsequent challenge.

Authors

JVJohn L. VanCottMMMonica McNealACAnthony H.-C. Choi

Discussion

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Overview

Animal data on Stat1 and rotavirus warrant no practice change; leaves open its role in human innate immunity and clearance.

Structured PICO

P
Population
Suckling and adult Stat1 knock-out mice and immunocompetent wild-type mice evaluated for rotavirus-induced diarrhea, viral replication, and immune protection.
E
Exposure
Oral infection with rotavirus or vaccination with rotavirus VP6 protein and mucosal adjuvant Escherichia coli heat-labile toxin LT (R192G)
C
Comparator
Immunocompetent (WT) mice or unimmunized controls
O
Outcome
Rotavirus-induced diarrhea and viral shedding (replication)surrogate

Loss of Stat1 causes a defective innate immune response in adult mice leading to increased viral shedding, but does not impair eventual viral clearance or protection against subsequent rotavirus challenge.

Cite This Study

VanCott et al. (2003) studied Rotavirus infection. Stat1 knock-out (loss of IFN function) vs. Immunocompetent wild-type mice was evaluated on Rotavirus shedding and diarrhea. Loss of Stat1 in adult mice resulted in up to 100-fold more rotavirus shedding compared to wild-type mice, but did not impair viral clearance or protection against subsequent challenge.

synapsesocial.com/papers/6a64bd724b71df2905b14e3bhttps://doi.org/10.1089/107999003321532501
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