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Fate of mRNA of L-cells infected with mengovirus
Abstract:
Mengovirus infection of L-cells results in an inhibition of host protein synthesis which is detectable in vivo by a decreased rate of incorporation of radioactive amino acids into acid-insoluble material and by a concomitant reduction in polysome content. The inhibition of host protein synthesis occurs early in the infection cycle, at a time when there is little synthesis of viral proteins. In this paper the stability of polyadenylic acid [poly(A)]-containing mRNA of uninfected L-cells and cells infected with mengovirus is compared. Our results suggest that there is no increase in the rate of degradation of cellular mRNA upon virus infection. The continued integrity of host mRNA throughout infection was verified by acrylamide gel electrophoresis.
Insights
Mengovirus infection halts host protein synthesis in L-cells. However, cellular messenger RNA (mRNA) remains stable, indicating the inhibition is not due to mRNA degradation.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Mengovirus infection of L-cells inhibits host protein synthesis early in the infection cycle.
- This inhibition is characterized by reduced amino acid incorporation and polysome content.
- Viral protein synthesis is minimal when host protein synthesis is inhibited.
Purpose of the Study:
- To investigate the stability of polyadenylic acid [poly(A)]-containing messenger RNA (mRNA) in L-cells during mengovirus infection.
- To determine if increased degradation of cellular mRNA contributes to the inhibition of host protein synthesis.
Main Methods:
- Comparing the stability of poly(A)-containing mRNA in uninfected and mengovirus-infected L-cells.
- Analyzing mRNA integrity using acrylamide gel electrophoresis.
Main Results:
- No significant increase in the degradation rate of cellular mRNA was observed in infected cells compared to uninfected cells.
- The integrity of host mRNA was maintained throughout the infection process.
- This suggests that cellular mRNA remains intact despite the inhibition of host protein synthesis.
Conclusions:
- The inhibition of host protein synthesis during mengovirus infection is not caused by accelerated degradation of cellular mRNA.
- Cellular mRNA integrity is preserved, implying other mechanisms are responsible for the observed translational shutoff.