Population
Intestinal cell lines (HT-29, Caco-2, and MA104)
Comparison
Rotavirus infection or UV-psoralen-inactivated… vs Uninfected cells or cells without inhibitors
Design
Preclinical
Authors
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Should not change rotavirus management; leaves open JNK/p38 inhibition as hypothesis-generating antiviral strategy requiring in vivo validation.
Rotavirus infection activates JNK and p38 signaling pathways, which are required for AP-1-driven gene expression and optimal viral replication in intestinal cells.
Holloway et al. (2006) studied this question.
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