Two mutations in the vif gene of maedi-visna virus have different phenotypes, indicating more than one function of Vif

Sigrídur R. Franzdóttir, Katrín Ólafsdóttir, Stefán R. Jónsson, Hannah Strobel, Ólafur S. Andrésson, Valgerdur Andrésdóttir*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)

Abstract

Like most other lentiviruses, maedi-visna virus (MVV) requires Vif for replication in natural target cells and in vivo. Here, we show that Vif-deficient MVV accumulates G-A mutations in the sequence context characteristic of ovine APOBEC3, consistent with a role of MVV Vif in neutralizing APOBEC3. We studied two point mutations in the vif gene of MVV. One was a tryptophan to arginine mutation that affects the interaction with APOBEC3 and caused G-A hypermutation. The other mutation was a proline to serine mutation that together with a mutation in the capsid protein caused attenuated replication in fetal ovine synovial (FOS) cells but not in sheep choroid plexus (SCP) cells. There was no hypermutation associated with this mutation. These results suggest that MVV Vif exerts more than one function and that there may be interaction between Vif and the capsid. The results also suggest the involvement of an unknown host factor in MVV Vif function.

Original languageEnglish
Pages (from-to)37-42
Number of pages6
JournalVirology
Volume488
DOIs
Publication statusPublished - 15 Jan 2016

Bibliographical note

Funding Information:
This study was supported by the Icelandic Research Fund (Grant nos. 070453-021 and 141085-052 ) and the University of Iceland Research Fund .

Publisher Copyright:
© 2015 Elsevier Inc.

Other keywords

  • APOBEC3
  • Capsid
  • Host restriction
  • Lentivirus
  • Maedi-visna virus
  • Vif

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