The vif gene of maedi-visna virus is essential for infectivity in vivo and in vitro

Kristbjörnsdóttir, Helga Bryndı́s; Andrésdóttir, Valgerður; Svansson, Vilhjálmur; Torsteinsdóttir, Sigurbjörg; Matthíasdóttir, Sigríður; Andrésson, Ólafur S.

doi:10.1016/j.virol.2003.09.044

Cited by 24 publications

(22 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is found in the cytoplasm and is not incorporated into the virion [42,154]. In VMV, replication of a vif-deleted virus is severely affected in macrophages and is non-infectious in sheep [155]. This mutant also accumulates G to A mutations suggesting a similar function for VIF as in HIV, i.e.…”

Section: Replicationmentioning

confidence: 99%

Small Ruminant Lentiviruses and Human Immunodeficiency Virus: Cousins that Take a Long View

Blacklaws

Harkiss²

2010

CHR

View full text Add to dashboard Cite

Small ruminant lentiviruses (SRLV) and human immunodeficiency viruses (HIV) are related retroviruses that cause multisystem disease usually over a long period of time. The viruses show similarities and differences in biological and pathogenic features. The basic retroviral genomic organization is complicated by the presence of a variable number of accessory genes in both viruses, though the structure is more complex in HIV. Both are mucosal pathogens, and infect cells of the monocyte-macrophage lineage. The main difference in cell tropism is that, unlike HIV, SRLV do not infect lymphocytes. A major feature of both pathogens is restricted replication and virus latency, which are partly responsible for the establishment of chronic infection usually lasting for life. The pathologies observed are similar in the early stages of both infections, and possibly following highly active anti-retroviral therapy (HAART). While the pathogenesis of HIV-induced disease during symptomatic stages is mainly due to secondary infections and neoplastic conditions, the early and post-HAART stages are associated with chronic inflammatory changes that resemble those found in SRLV diseases which are thought to be mediated by anti-virus immune responses.

show abstract

Section: Replicationmentioning

confidence: 99%

Small Ruminant Lentiviruses and Human Immunodeficiency Virus: Cousins that Take a Long View

Blacklaws

Harkiss²

2010

CHR

View full text Add to dashboard Cite

show abstract

“…A similar phenotype was obtained for other Vif (= Vif deleted) lentiviruses including HIV-2, simian immunodeficiency virus (SIV), feline immunodeficiency virus (FIV), caprine arthritis encephalitis virus (CAEV), and Maedi-visna virus (MVV, [84,126,137,192,212,233,302,347]). Equine infectious anemia virus (EIAV) is the only lentivirus that does not encode vif [246].…”

Section: Antiviral Defense By Cellular Cytidine-deaminases the Role Omentioning

confidence: 53%

“…Maedi-visna virus, a lentivirus of sheep, encodes a Vif gene. G->A hypermutations are observed if Vif is inactivated [192]. How EIAV, the only lentivirus that lacks a vif-gene, escapes APOBEC-mediated deamination is unknown.…”

Section: Effect Of Apobec-family Members On Other Retrovirusesmentioning

confidence: 99%

Intracellular Restriction Factors In Mammalian Cells - An Ancient Defense System Finds A Modern Foe

Baumann¹

2006

CHR

View full text Add to dashboard Cite

Cross-species transmission of retroviruses poses a threat to mammalian species. Zoonoses have given rise to devastating diseases because the host organism is not prepared to resist a new pathogen. Mammals have developed several layers of defense against viruses, including an intracellular antiretroviral defense, a part of innate immunity. Retroviral restrictions had been studied for decades using murine leukemia virus in mice, however it has become clear that primates too have intrinsic mechanisms to ward off infections by retroviruses. Several of these antiretroviral restriction mechanisms have recently been identified, with two particularly well described factors being members of the tripartite motif (Trim) and APOBEC families. Both systems provide a strong barrier against lentiviral infections. The viruses have developed countermeasures that allow them to replicate despite the host factors. This review discusses our current knowledge of this ancient battle between mammalian hosts and their retroviral opponents.

show abstract

“…Thus, Vifdeficient MVV replicates poorly in macrophages and sheep choroid plexus (SCP) cells, whereas fetal ovine synovial (FOS) cells appear semipermissive. We have also found an elevated frequency of G3A mutations in Vif-deficient MVV, indicating a function for MVV Vif that is similar to that of human immunodeficency virus type 1 (HIV-1) (18).…”

mentioning

confidence: 67%

“…The vif gene, which is present in all lentiviruses except equine infectious anemia virus, counteracts APOBEC3G by causing its degradation. Vif is essential for virus infectivity in vivo and for replication in primary cells in vitro (5,12,13,18,20,31).…”

mentioning

confidence: 99%

Simultaneous Mutations in CA and Vif of Maedi-Visna Virus Cause Attenuated Replication in Macrophages and Reduced Infectivity In Vivo

Gudmundsson

Jónsson

Ólafsson

et al. 2005

J Virol

View full text Add to dashboard Cite

Maedi-visna virus (MVV) is a lentivirus of sheep sharing several key features with the primate lentiviruses.The virus causes slowly progressive diseases, mainly in the lungs and the central nervous system of sheep. Here, we investigate the molecular basis for the differential growth phenotypes of two MVV isolates. One of the isolates, KV1772, replicates well in a number of cell lines and is highly pathogenic in sheep. The second isolate, KS1, no longer grows on macrophages or causes disease. The two virus isolates differ by 129 nucleotide substitutions and two deletions of 3 and 15 nucleotides in the env gene. To determine the molecular nature of the lesions responsible for the restrictive growth phenotype, chimeric viruses were constructed and used to map the phenotype. An L120R mutation in the CA domain, together with a P205S mutation in Vif (but neither alone), could fully convert KV1772 to the restrictive growth phenotype. These results suggest a functional interaction between CA and Vif in MVV replication, a property that may relate to the innate antiretroviral defense mechanisms in sheep.

show abstract

The vif gene of maedi-visna virus is essential for infectivity in vivo and in vitro

Cited by 24 publications

References 57 publications

Small Ruminant Lentiviruses and Human Immunodeficiency Virus: Cousins that Take a Long View

Small Ruminant Lentiviruses and Human Immunodeficiency Virus: Cousins that Take a Long View

Intracellular Restriction Factors In Mammalian Cells - An Ancient Defense System Finds A Modern Foe

Simultaneous Mutations in CA and Vif of Maedi-Visna Virus Cause Attenuated Replication in Macrophages and Reduced Infectivity In Vivo

Contact Info

Product

Resources

About