ArticleProceedings of the National Academy of Sciences of the United States of America2013
Antagonism of SAMHD1 is actively maintained in natural infections of simian immunodeficiency virus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Deciphering lentiviral Vpr/Vpx determinants required for HUSH and SAMHD1 antagonism highlights the molecular plasticity of these evolutionary conflicts.Journal of virology · 2025Article
- Review
- Role of Intracellular Distribution of Feline and Bovine SAMHD1 Proteins in Lentiviral Restriction.Virologica Sinica · 2021Article
- Structural insights into Cullin4-RING ubiquitin ligase remodelling by Vpr from simian immunodeficiency viruses.PLoS pathogens · 2021Article
- Vpx enhances innate immune responses independently of SAMHD1 during HIV-1 infection.Retrovirology · 2021Article
- HIV-1 Vpr induces cell cycle arrest and enhances viral gene expression by depleting CCDC137.eLife · 2020Article
- Ubiquitination and SUMOylation in HIV Infection: Friends and Foes.Current issues in molecular biology · 2020Review
- Article
- Review
- Positive selection in dNTPase SAMHD1 throughout mammalian evolution.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Interplay of ancestral non-primate lentiviruses with the virus-restricting SAMHD1 proteins of their hosts.The Journal of biological chemistry · 2018Article
- Host SAMHD1 protein restricts endogenous reverse transcription of HIV-1 in nondividing macrophages.Retrovirology · 2018Article
- Recurrent Loss of APOBEC3H Activity during Primate Evolution.Journal of virology · 2018Article
- Systemic HIV-1 infection produces a unique glial footprint in humanized mouse brains.Disease models & mechanisms · 2017Article
- The KT Jeang Retrovirology prize 2017: Michael Emerman.Retrovirology · 2017Article
- Natural mutations in IFITM3 modulate post-translational regulation and toggle antiviral specificity.EMBO reports · 2016Article
- Molecular determinants for recognition of divergent SAMHD1 proteins by the lentiviral accessory protein Vpx.Cell host & microbe · 2015Article
- G2/M cell cycle arrest correlates with primate lentiviral Vpr interaction with the SLX4 complex.Journal of virology · 2015Article
- Article
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Restriction factors are effectors of the innate immune response to viral pathogens that inhibit viral replication by operating as molecular barriers to steps of the viral life cycle. The restriction factor SAMHD1 blocks lentiviral reverse transcription in myeloid cells and resting CD4+ T cells. Many lineages of lentiviruses, including HIV-2 and other simian immunodeficiency viruses, encode accessory genes that serve to counteract host SAMHD1 restriction by causing degradation of the antiviral factor. The viral accessory protein Vpr is responsible for SAMHD1 degradation in some lineages of lentiviruses, whereas in others the related protein Vpx assumes this task. However, HIV-1 has no SAMHD1 degradation capability, leading to questions about the selective advantage of this activity. We use an evolutionary approach to examine the importance of SAMHD1 antagonism for viral fitness by studying adaptation to host SAMHD1 in natural simian immunodeficiency virus infections of African Green Monkeys. We identified multiple SAMHD1 haplotypes in African Green Monkeys and find that the vpr gene from different strains of Simian Immunodeficiency Virus has adapted to the polymorphisms of the African Green Monkey population in which it is found. Such evidence of viral adaptation to host restriction indicates that SAMHD1 antagonism is actively maintained in natural infections and that this function must be advantageous to viral fitness, despite its absence in HIV-1.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.