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Differential inhibition of cellular and Sindbis virus translation by brefeldin A

Susana Molina1, Miguel A Sanz, Vanesa Madan

  • 1Centro de Biología Molecular CSIC-UAM, Facultad de Ciencias, Universidad Autónoma, Cantoblanco, 28049 Madrid, Spain. smolina@cbm.uam.es <smolina@cbm.uam.es>

Virology
|March 16, 2007
PubMed

Insights

Brefeldin A inhibits cellular protein synthesis but not Sindbis virus protein synthesis. This macrolide compound delays viral RNA replication but does not directly impact viral protein synthesis.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Brefeldin A (BFA) is a macrolide antibiotic impacting cellular secretory pathways and protein synthesis.
  • BFA inhibits viral glycoprotein maturation and genome replication in enveloped viruses.

Purpose of the Study:

  • To investigate the effect of BFA on Sindbis virus (SINV) protein synthesis and replication.
  • To determine if SINV translation is affected by BFA-induced cellular stress.

Main Methods:

  • Treatment of mammalian cells with BFA.
  • Analysis of viral and cellular protein synthesis using SINV.
  • Assessment of SINV RNA replication using a SINV replicon system.
  • Monitoring of eukaryotic initiation factor 2 alpha (eIF2alpha) phosphorylation.

Main Results:

  • Prolonged BFA treatment inhibited cellular translation but not SINV subgenomic mRNA translation.
  • BFA-induced eIF2alpha phosphorylation correlated with cellular translation inhibition, but late viral protein synthesis remained resistant.
  • BFA delayed SINV RNA synthesis in a replicon system, but translation of non-replicative viral RNAs was unaffected.

Conclusions:

  • SINV protein synthesis is resistant to BFA, suggesting a mechanism independent of cellular translation inhibition.
  • BFA primarily affects viral RNA replication rather than directly inhibiting SINV protein synthesis.
  • These findings highlight distinct cellular responses to BFA in viral replication and protein synthesis.

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