Rapamycin and Wortmannin Enhance Replication of a Defective Encephalomyocarditis Virus
Why the study?
Do rapamycin and wortmannin enhance the replication of defective Encephalomyocarditis virus in BHK-21 cells?
Population
BHK-21 cells infected with defective Encephalomyocarditis virus strains generated by deleting portions of…
Comparison
Rapamycin and wortmannin vs Absence of rapamycin and wortmannin
Design
Preclinical
Authors
Discussion
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Implication
Hypothesis-generating for PI3K-FRAP inhibition in EMCV replication; leaves open in vivo relevance and clinical antiviral implications.
Structured PICO
Do rapamycin and wortmannin enhance the replication of defective Encephalomyocarditis virus in BHK-21 cells?
P
Population
BHK-21 cells infected with defective Encephalomyocarditis virus (EMCV) strains generated by deleting portions of the 2A coding region
I
Intervention
Rapamycin and wortmannin (inhibitors of the PI3 kinase-FRAP pathway)
C
Comparator
Absence of rapamycin and wortmannin
O
Outcome
Viral protein synthesis, host translation shutoff, and yield of mutant virusessurrogate
Inhibition of the PI3 kinase-FRAP signaling pathway by rapamycin and wortmannin partly complements mutations in the 2A protein of EMCV, reversing a slow-virus phenotype.
Cite This Study
Svitkin et al. (1998) studied this question.