Literature DB >> 22522310

Endogenous lentiviral elements in the weasel family (Mustelidae).

Guan-Zhu Han1, Michael Worobey.   

Abstract

Endogenous retroviruses provide molecular fossils for studying the ancient evolutionary history of retroviruses. Here, we report our independent discovery and analysis of endogenous lentiviral insertions (Mustelidae endogenous lentivirus [MELV]) within the genomes of weasel family (Mustelidae). Genome-scale screening identified MELV elements in the domestic ferret (Mustela putorius furo) genome (MELVmpf). MELVmpf exhibits a typical lentiviral genomic organization. Phylogenetic analyses position MELVmpf basal to either primate lentiviruses or feline immunodeficiency virus. Moreover, we verified the presence of MELV insertions in the genomes of several species of the Lutrinae and Mustelinae subfamilies but not the Martinae subfamily, suggesting that the invasion of MELV into the Mustelidae genomes likely took place between 8.8 and 11.8 Ma. The discovery of MELV in weasel genomes extends the host range of lentiviruses to the Caniformia (order Carnivora) and provides important insights into the prehistoric diversity of lentiviruses.

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Mesh:

Year:  2012        PMID: 22522310      PMCID: PMC3457773          DOI: 10.1093/molbev/mss126

Source DB:  PubMed          Journal:  Mol Biol Evol        ISSN: 0737-4038            Impact factor:   16.240


  19 in total

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7.  Endogenous lentiviruses in the ferret genome.

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  22 in total

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Review 5.  Host gene evolution traces the evolutionary history of ancient primate lentiviruses.

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7.  An endogenous foamy-like viral element in the coelacanth genome.

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8.  Evolutionary and Functional Analysis of Old World Primate TRIM5 Reveals the Ancient Emergence of Primate Lentiviruses and Convergent Evolution Targeting a Conserved Capsid Interface.

Authors:  Kevin R McCarthy; Andrea Kirmaier; Patrick Autissier; Welkin E Johnson
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9.  Convergence and divergence in the evolution of the APOBEC3G-Vif interaction reveal ancient origins of simian immunodeficiency viruses.

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10.  Gain-of-sensitivity mutations in a Trim5-resistant primary isolate of pathogenic SIV identify two independent conserved determinants of Trim5α specificity.

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