Key Points
- Determine whether the 2'-5'-oligoadenylate synthetase-RNase L pathway mediates beta interferon-induced inhibition of encephalomyocarditis virus replication in mouse cell lines.
- Isolated clonal derivatives (selected clone RK8 and unselected clone RK6) from parental mouse JLSV-11 cells based on rescue by interferon from viral cytopathology.
- Quantified 2'-5'-oligoadenylate synthetase mRNA and enzyme activity alongside RNase L levels using radiolabeled 2'-5'-oligoadenylate binding and cross-linking assays.
- Assessed protein synthesis inhibition and replication efficiency of encephalomyocarditis virus, vesicular stomatitis virus, and endogenous murine leukemia virus after interferon exposure.
- Both RK6 and RK8 cell clones exhibited similar elevations in 2'-5'-oligoadenylate synthetase mRNA and enzyme activity following interferon exposure.
- RNase L levels were markedly lower in RK6 cells than in RK8 cells, corresponding to substantially weaker protein synthesis inhibition upon direct introduction of 2'-5'-oligoadenylates in RK6.
- Interferon inhibited replication of both vesicular stomatitis virus and encephalomyocarditis virus in RK8 cells, but failed to inhibit encephalomyocarditis virus replication in RNase L-deficient RK6 cells.
Structured PICO
PPopulationMouse JLSV-11 cells and clonal derivatives (RK8 and RK6)
IInterventionInterferon treatment and introduction of 2'-5'-oligoadenylates
CComparatorComparison between interferon-responsive clone (RK8) and non-responsive clone (RK6)
OOutcomeInhibition of encephalomyocarditis virus (EMCV) and vesicular stomatitis virus (VSV) replicationsurrogate
The 2'-5'-oligoadenylate-dependent RNase L pathway appears to mediate the inhibition of encephalomyocarditis virus replication by interferons in mouse cells.