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

Autor: Franzdóttir SR; Institute for Experimental Pathology, Keldur, University of Iceland, Reykjavik, Iceland., Ólafsdóttir K; Institute for Experimental Pathology, Keldur, University of Iceland, Reykjavik, Iceland., Jónsson SR; Institute for Experimental Pathology, Keldur, University of Iceland, Reykjavik, Iceland., Strobel H; Institute for Experimental Pathology, Keldur, University of Iceland, Reykjavik, Iceland., Andrésson ÓS; Faculty of Life and Environmental Sciences, University of Iceland, Iceland., Andrésdóttir V; Institute for Experimental Pathology, Keldur, University of Iceland, Reykjavik, Iceland. Electronic address: valand@hi.is.
Jazyk: angličtina
Zdroj: Virology [Virology] 2016 Jan 15; Vol. 488, pp. 37-42. Date of Electronic Publication: 2015 Nov 17.
DOI: 10.1016/j.virol.2015.10.035
Abstrakt: 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.
(Copyright © 2015 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
Externí odkaz: