Simian immunodeficiency virus SIVagm from African green monkeys does not antagonize endogenous levels of African green monkey tetherin/BST-2.

Publication Type:

Journal Article

Source:

Journal of virology, Volume 83, Issue 22, p.11673-81 (2009)

Keywords:

2009, Animals, Blotting, Western, Cell Line, Center-Authored Paper, Cercopithecus aethiops, Flow Cytometry Core Facility, Gene Products, nef, Genomics Core Facility, Human Biology Division, Interferon Alfa-2a, Interferon-beta, Molecular Sequence Data, Retroviridae Proteins, Reverse Transcriptase Polymerase Chain Reaction, Shared Resources, Simian Acquired Immunodeficiency Syndrome, Simian immunodeficiency virus, Viral Regulatory and Accessory Proteins

Abstract:

The Vpu accessory gene that originated in the primate lentiviral lineage leading to human immunodeficiency virus type 1 is an antagonist of human tetherin/BST-2 restriction. Most other primate lentivirus lineages, including the lineage represented by simian immunodeficiency virus SIVagm from African green monkeys (AGMs), do not encode Vpu. While some primate lineages encode gene products other than Vpu that overcome tetherin/BST-2, we find that SIVagm does not antagonize physiologically relevant levels of AGM tetherin/BST-2. AGM tetherin/BST-2 can be induced by low levels of type I interferon and can potently restrict two independent strains of SIVagm. Although SIVagm Nef had an effect at low levels of AGM tetherin/BST-2, simian immunodeficiency virus SIVmus Vpu, from a virus that infects the related monkey Cercopithecus cephus, is able to antagonize even at high levels of AGM tetherin/BST-2 restriction. We propose that since the replication of SIVagm does not induce interferon production in vivo, tetherin/BST-2 is not induced, and therefore, SIVagm does not need Vpu. This suggests that primate lentiviruses evolve tetherin antagonists such as Vpu or Nef only if they encounter tetherin during the typical course of natural infection.