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Schlafen 11 Restricts Flavivirus Replication.

Federico Valdez1, Julienne Salvador1, Pedro M Palermo1

  • 1Department of Biological Sciences, The University of Texas at El Paso, El Paso, Texas, USA.

Journal of Virology
|May 24, 2019
PubMed
Summary
This summary is machine-generated.

The cellular protein Schlafen 11 (Slfn11) restricts flavivirus replication, including West Nile virus, dengue virus, and Zika virus. Slfn11 impairs viral infectivity by preventing modifications to host tRNAs essential for viral protein folding.

Keywords:
Schlafen 11flavivirusvirus restriction factors

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Schlafen 11 (Slfn11) is an interferon-stimulated gene regulating protein synthesis via tRNA abundance.
  • Slfn11 has been shown to inhibit HIV-1 infection and the expression of codon-biased open reading frames.

Purpose of the Study:

  • To investigate the differential sensitivity of positive-sense single-stranded RNA [(+)ssRNA] and negative-sense single-stranded RNA [(-)ssRNA] viruses to Slfn11.
  • To determine the effect of Slfn11 on the replication of various ssRNA viruses in human glioblastoma cells.

Main Methods:

  • Tested Slfn11's effect on (+)ssRNA (WNV, DENV, ZIKV) and (-)ssRNA (VSV, RVFV) virus replication in A172 cells.
  • Depleted Slfn11 to assess its impact on viral replication.
  • Quantified viral particles to PFU ratio to evaluate WNV infectivity.
  • Analyzed tRNA downregulation in WNV-infected cells with and without Slfn11.

Main Results:

  • Slfn11 depletion significantly enhanced replication of (+)ssRNA flaviviruses (WNV, DENV, ZIKV).
  • Slfn11 had no significant effect on (-)ssRNA viruses (VSV, RVFV).
  • Slfn11 was found to impair WNV infectivity and prevent WNV-induced tRNA downregulation.

Conclusions:

  • Slfn11 acts as a cellular restriction factor against flavivirus replication by impairing viral infectivity.
  • Slfn11's mechanism involves preventing virus-induced alterations in the host tRNA repertoire, potentially affecting viral protein folding.
  • Slfn11 is not the limiting factor in this antiviral pathway.