Key Points
- To determine whether poliovirus-mediated inhibition of cellular protein secretion via the viral 3A protein affects the release of antiviral and proinflammatory cytokines.
- Assayed cytokine secretion in cells infected with wild-type poliovirus versus the 3A-2 mutant carrying an insertion in protein 3A that impairs secretory pathway inhibition.
- Compared viral replication kinetics, host cell translation shutdown, and transcriptional induction of beta interferon mRNA between wild-type and 3A-2-infected cells.
- Cells infected with the 3A-2 mutant virus secreted significantly greater amounts of interleukin-6, interleukin-8, and beta interferon than wild-type poliovirus-infected cells.
- Wild-type and 3A-2 mutant viruses showed equivalent rates of viral growth, host translation inhibition, and induction of beta interferon mRNA transcripts.
Structured PICO
PPopulationCells infected with poliovirus
IInterventionInfection with 3A-2 mutant poliovirus (carrying an insertion in viral protein 3A rendering it defective in the inhibition of protein secretion)
CComparatorInfection with wild-type poliovirus
OOutcomeSecretion of cytokines interleukin-6 (IL-6), IL-8, and beta interferonsurrogate
The poliovirus 3A protein inhibits host protein secretion, reducing the release of proinflammatory and antiviral cytokines, which may serve as a mechanism to evade the native immune response.