Key result
Rotavirus infection induces the phosphorylation of eIF2α but prevents the formation of stress granules, allowing the translation of viral mRNAs while shutting off cellular protein synthesis.
Population
Cells infected with rotavirus (including wild-type and mutant cells producing nonphosphorylatable eIF2alpha)
Comparison
Rotavirus infection and RNA interference… vs Uninfected cells and wild-type cells
Design
Preclinical
Authors
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Animal data suggest rotavirus evasion strategies as antiviral targets; leaves open human translation and therapeutic testing.
Rotavirus evades cellular translational shutoff mechanisms by preventing stress granule formation despite inducing eIF2alpha phosphorylation.
Montero et al. (2007) studied Rotavirus infection (in vitro). Rotavirus infection vs. Mock infection was evaluated on Phosphorylation of eIF2α and stress granule formation. Rotavirus infection induces the phosphorylation of eIF2α but prevents the formation of stress granules, allowing the translation of viral mRNAs while shutting off cellular protein synthesis.
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