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Phospholipid synthesis in Sindbis virus-infected cells
Journal of Virology
|November 1, 1970
Summary
Sindbis virus infection inhibits phospholipid synthesis in chick cells, requiring viral RNA synthesis but not viral proteins. This inhibition is likely a secondary effect of the virus disrupting host cell RNA and protein production.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Background:
- Previous studies observed decreased phospholipid synthesis in chick embryo fibroblasts infected with Sindbis virus.
- The specific metabolic requirements for this observed inhibition were not fully understood.
Purpose of the Study:
- To investigate the metabolic requirements for Sindbis virus-induced inhibition of phospholipid synthesis.
- To determine the role of viral RNA and protein synthesis in this process.
Main Methods:
- Utilized (32)PO(4) and (14)C-choline incorporation to measure phospholipid synthesis.
- Employed temperature-sensitive Sindbis virus mutants to assess the necessity of viral RNA and protein synthesis.
- Compared effects of actinomycin D and cycloheximide on choline incorporation in infected and uninfected cells.
Main Results:
- Viral ribonucleic acid (RNA) synthesis was essential for inhibiting choline incorporation, but functional viral structural proteins were not.
- Inhibition of host cell RNA and protein synthesis preceded the decline in phospholipid synthesis.
- Actinomycin D and cycloheximide inhibited choline incorporation in uninfected cells, suggesting a broader impact on synthesis pathways.
Conclusions:
- The decrease in phospholipid synthesis during Sindbis virus infection is likely a secondary effect of viral inhibition of host cell RNA and protein synthesis.
- Viral RNA synthesis is a key factor in triggering these inhibitory effects.
- The response of phospholipid synthesis to Sindbis virus differs between cell types, with BHK cells showing late inhibition.