ArticleScientific reports2016
SAMHD1 transcript upregulation during SIV infection of the central nervous system does not associate with reduced viral load.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Role of Intracellular Distribution of Feline and Bovine SAMHD1 Proteins in Lentiviral Restriction.Virologica Sinica · 2021Article
- Insights into the Gene Expression Profiles of Active and Restricted Red/Green-HIVJournal of virology · 2020Article
- SAMHD1 as the Potential Link Between SARS-CoV-2 Infection and Neurological Complications.Frontiers in neurology · 2020Review
- Increased SAMHD1 transcript expression correlates with interferon-related genes in HIV-1-infected patients.Medical microbiology and immunology · 2019Article
- The role of SAMHD1 expression and its relation to HIV-2 (Vpx) gene production.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2018Review
- Interferons Induce Expression of SAMHD1 in Monocytes through Down-regulation of miR-181a and miR-30a.The Journal of biological chemistry · 2017Article
- Immune Activation Influences SAMHD1 Expression and Vpx-mediated SAMHD1 Degradation during Chronic HIV-1 Infection.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Restriction of HIV-1 in myeloid-lineage cells is attributed in part to the nucleotidase activity of the SAM-domain and HD-domain containing protein (SAMHD1), which depletes free nucleotides, blocking reverse transcription. In the same cells, the Vpx protein of HIV-2 and most SIVs counteracts SAMHD1. Both Type I and II interferons may stimulate SAMHD1 transcription. The contributions of SAMHD1 to retroviral restriction in the central nervous system (CNS) have been the subject of limited study. We hypothesized that SAMHD1 would respond to interferon in the SIV-infected CNS but would not control virus due to SIV Vpx. Accordingly, we investigated SAMHD1 transcript abundance and association with the Type I interferon response in an SIV model. SAMHD1 transcript levels were IFN responsive, increasing during acute phase infection and decreasing during a more quiescent phase, but generally remaining elevated at all post-infection time points. In vitro, SAMHD1 transcript was abundant in macaque astrocytes and further induced by Type I interferon, while IFN produced a weaker response in the more permissive environment of the macrophage. We cannot rule out a contribution of SAMHD1 to retroviral restriction in relatively non-permissive CNS cell types. We encourage additional research in this area, particularly in the context of HIV-1 infection.
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Registered trials
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.