COVID-19 is an emerging, rapidly evolving situation.

Get the latest public health information from CDC: https://www.coronavirus.gov
Get the latest research information from NIH: https://www.nih.gov/coronavirus
Find NCBI SARS-CoV-2 literature, sequence, and clinical content: https://www.ncbi.nlm.nih.gov/sars-cov-2/

Virology. 2020 Dec 29;555 78-88. doi: 10.1016/j.virol.2020.12.015. Online ahead of print.
Human Schlafen 11 exploits codon preference
discrimination to attenuate viral protein synthesis of
prototype foamy virus (PFV)
Ge Guo  1 , Yang Wang  1 , Xiao-Mei Hu  1 , Zhuo-Ran Li  1 , Juan Tan  1 , Wen-Tao Qiao   2
Affiliations
PMID: 33465725 DOI: 10.1016/j.virol.2020.12.015
Abstract
Recently, the Schlafen (SLFN) proteins have been identified as a novel interferon-stimulated family
with antiviral properties. In this study, we reported that SLFN11 inhibited prototype foamy virus
(PFV) replication. Over-expression of human SLFN11 reduced viral production, while knockdown of
SLFN11 enhanced viral infectivity. In addition, SLFN11 from cattle and African green monkey also
suppressed PFV production. Both the ATPase activity and helicase activity of SLFN11 were required
for its inhibitory function. Dephosphorylation activated the antiviral activity of SLFN11. More
importantly, SLFN11 inhibited the expression of viral protein, which was rescued by viral gene
codon optimization. Together, our results demonstrated that SLFN11 impaired PFV viral protein
synthesis by exploiting the distinct codon usage between the virus and the host. These findings
further broaden our understanding of the antiviral properties of the SLFN family and the molecular
mechanism of PFV latent infection.
Keywords: Antivirus; Codon bias; Prototype foamy virus; SLFN11.
Copyright © 2020. Published by Elsevier Inc.