Why the study?
No approved antiviral compounds or vaccines exist for EV-D68, and an appropriate mouse model is needed to develop therapeutics.
Population
AGB6, AB6, GB6, parental B6, and AGB6-Setd3 mice
Comparison
EV-D68 infection across strains and Setd3 genotypes
Design
Preclinical animal model study
Key result
While EV-D68 lethality was completely penetrant in wild-type and heterozygous mice, all AGB6-Setd3-/- littermates survived, indicating SETD3 is essential for EV-D68 pathogenesis.
Authors
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AG129 mice support preclinical EV-D68 antiviral screening; leaves open translation to human AFM therapies.
Absolute Event Rate: 100% vs 0%
SETD3 is essential for EV-D68 pathogenesis in a novel AGB6 mouse model, highlighting it as a promising therapeutic target for enterovirus infections.
Watarastaporn et al. (2024) studied EV-D68 acute flaccid myelitis (mouse model). Setd3 knockout (AGB6-Setd3-/- mice) vs. AGB6-Setd3+/+ and AGB6-Setd3+/- mice was evaluated on Survival / EV-D68 lethality. While EV-D68 lethality was completely penetrant in wild-type and heterozygous mice, all AGB6-Setd3-/- littermates survived, indicating SETD3 is essential for EV-D68 pathogenesis.