ArticleRetrovirology2013
Evidence for IFNα-induced, SAMHD1-independent inhibitors of early HIV-1 infection.
Article in Retrovirology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 56 citations in OpenAlex.
- Host cell restriction factors of equine infectious anemia virus.Virologica Sinica · 2023Review
- The DEAD box RNA helicase DDX42 is an intrinsic inhibitor of positive-strand RNA viruses.EMBO reports · 2022Article
- The KT Jeang Retrovirology prize 2022: Florence Margottin-Goguet.Retrovirology · 2022Article
- Differential Inhibition of HIV Replication by the 12 Interferon Alpha Subtypes.Journal of virology · 2021Article
- Human Beta-Defensin 2 and 3 Inhibit HIV-1 Replication in Macrophages.Frontiers in cellular and infection microbiology · 2021Article
- SAMHD1 Functions and Human Diseases.Viruses · 2020Review
- Interferon γ and α Have Differential Effects on SAMHD1, a Potent Antiviral Protein, in Feline Lymphocytes.Viruses · 2019Article
- Increased SAMHD1 transcript expression correlates with interferon-related genes in HIV-1-infected patients.Medical microbiology and immunology · 2019Article
- SAMHD1 Suppression of Antiviral Immune Responses.Trends in microbiology · 2019Review
- Host SAMHD1 protein restricts endogenous reverse transcription of HIV-1 in nondividing macrophages.Retrovirology · 2018Article
- The aryl hydrocarbon receptor and interferon gamma generate antiviral states via transcriptional repression.eLife · 2018Article
- SAMHD1: Recurring roles in cell cycle, viral restriction, cancer, and innate immunity.Autoimmunity · 2018Review
- Type I interferon and HIV: Subtle balance between antiviral activity, immunopathogenesis and the microbiome.Cytokine & growth factor reviews · 2018Review
- Review
- Regulation of CD4 Receptor and HIV-1 Entry by MicroRNAs-221 and -222 during Differentiation of THP-1 Cells.Viruses · 2017Article
- Effects of Inner Nuclear Membrane Proteins SUN1/UNC-84A and SUN2/UNC-84B on the Early Steps of HIV-1 Infection.Journal of virology · 2017Article
- Targeting SAMHD1 with the Vpx protein to improve cytarabine therapy for hematological malignancies.Nature medicine · 2017Article
- Interferons Induce Expression of SAMHD1 in Monocytes through Down-regulation of miR-181a and miR-30a.The Journal of biological chemistry · 2017Article
- The Dynamic Interplay between HIV-1, SAMHD1, and the Innate Antiviral Response.Frontiers in immunology · 2017Review
- IFN-JCI insight · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundType I interferon (IFN) treatment of some cells, including dendritic cells, macrophages and monocytic THP-1 cells, restricts HIV-1 infection and prevents viral cDNA accumulation. Sterile alpha motif and HD domain protein 1 (SAMHD1), a dGTP-regulated deoxynucleotide triphosphohydrolase, reduces HIV-1 infectivity in myeloid cells, likely by limiting dNTPs available for reverse transcription, and has been described as IFNα-inducible. Myeloid cell infection by HIV-1 is enhanced by HIV-2/SIVSM Vpx, which promotes SAMHD1 degradation, or by exogenous deoxyribonucleoside (dN) addition.
findingsSAMHD1 expression was not substantially influenced by IFNα treatment of monocyte-derived macrophages or THP-1 cells. The contributions of SAMHD1 to the inhibition of HIV-1 infectivity by IFNα were assessed through the provision of Vpx, exogenous dN addition, or via RNAi-mediated SAMHD1 knock-down. Both Vpx and dN efficiently restored infection in IFNα-treated macrophages, albeit not to the levels seen with these treatments in the absence of IFNα. Similarly using differentiated THP-1 cells, the addition of Vpx or dNs, or SAMHD1 knock-down, also stimulated infection, but failing to match the levels observed without IFNα. Neither Vpx addition nor SAMHD1 knock-down reversed the IFNα-induced blocks to HIV-1 infection seen in dividing U87-MG or THP-1 cells. Therefore, altered SAMHD1 expression or function cannot account for the IFNα-induced restriction to HIV-1 infection seen in many cells and cell lines.
conclusionIFNα establishes an anti-HIV-1 phenotype in many cell types, and appears to accomplish this without potentiating SAMHD1 function. We conclude that additional IFNα-induced suppressors of the early stages of HIV-1 infection await identification.
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