Enhanced ERK-1/2 activation in mice susceptible to coxsackievirus-induced myocarditis
Population
In vitro models and in vivo mouse models
Comparison
Group B coxsackievirus infection with or without… vs Uninfected controls, Lck-negative cells, or…
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Supports ERK-1/2/Src inhibition as antiviral target in CVB3 models; leaves open human translation and clinical testing.
Structured PICO
P
Population
In vitro models (Jurkat T cells, JCaM T cells, neonatal cardiac myocytes) and in vivo mouse models (myocarditis-susceptible A/J mice and myocarditis-resistant C57BL/6 mice)
I
Intervention
Group B coxsackievirus (CVB3) infection with or without ERK-1/2 inhibition (UO126) or Src inhibition (PP2)
C
Comparator
Uninfected controls, Lck-negative cells, or myocarditis-resistant C57BL/6 mice
O
Outcome
ERK-1/2 activation and CVB3 viral replication/titerssurrogate
ERK-1/2 activation downstream of Src kinases is necessary for efficient CVB3 replication and may contribute to differential host susceptibility to viral myocarditis.
Cite This Study
Opavsky et al. (2002) studied this question.