ArticleScientific reports2016
Restrictive influence of SAMHD1 on Hepatitis B Virus life cycle.
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 51 papers.
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Who cites it
51 citing papers in PubMed, 63 citations in OpenAlex.
- SAMHD1 depletion restricts SARS-CoV-2 infection by suppressing HNF1-dependent ACE2 expression in lung epithelial cells.PLoS pathogens · 2026Article
- Host restriction factor SAMHD1 does not restrict seasonal influenza virus replication in human epithelial or macrophage-like cells.Virology journal · 2026Article
- Dynamic changes in IFI44L and SAMHD1 mRNA levels in PBMCs are associated with treatment response in HBeAg-negative chronic hepatitis B during peg-IFN-α therapy.Frontiers in microbiology · 2026Article
- Hepatocyte SAMHD1 Deficiency Attenuates Hepatic Steatosis via Suppression of SREBP Activation in a Mouse Model of Metabolic-Associated Steatotic Liver Disease.International journal of biological sciences · 2026Article
- SAMHD1 promotes SARS-CoV-2 infection by enhancing HNF1-dependent ACE2 expression in lung epithelial cells.bioRxiv : the preprint server for biology · 2025Article
- Review
- Review
- Impaired influenza A virus replication by the host restriction factor SAMHD1 which inhibited by PA-mediated dephosphorylation of the host transcription factor IRF3.Virology journal · 2024Article
- A small molecule iCDM-34 identified by in silico screening suppresses HBV DNA through activation of aryl hydrocarbon receptor.Cell death discovery · 2023Article
- SAMHD1 impairs type I interferon induction through the MAVS, IKKε, and IRF7 signaling axis during viral infection.The Journal of biological chemistry · 2023Article
- The host antiviral protein SAMHD1 suppresses NF-κB activation by interacting with the IKK complex during inflammatory responses and viral infection.The Journal of biological chemistry · 2023Article
- The role of O-GlcNAcylation in innate immunity and inflammation.Journal of molecular cell biology · 2023Review
- Human cytomegalovirus UL24 and UL43 products participate in SAMHD1 subcellular localization.Virusdisease · 2022Article
- CK1α upregulates the IFNAR1 expression to prompt the anti-HBV effect of type I IFN in hepatoma carcinoma cells.Virologica Sinica · 2022Article
- Expression of SAMHD1 and its mutation on prognosis of colon cancer.Oncology letters · 2022Article
- The CCR5 Gene Edited CD34Frontiers in immunology · 2022Article
- RNR-R2 Upregulation by a Short Non-Coding Viral Transcript.Biomolecules · 2021Article
- The Balance between p53 Isoforms Modulates the Efficiency of HIV-1 Infection in Macrophages.Journal of virology · 2021Article
- SAMHD1 Inhibits Multiple Enteroviruses by Interfering with the Interaction between VP1 and VP2 Proteins.Journal of virology · 2021Article
- SAMHD1 … and Viral Ways around It.Viruses · 2021Review
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
Abstract
Deoxynucleotide triphosphates (dNTPs) are essential for efficient hepatitis B virus (HBV) replication. Here, we investigated the influence of the restriction factor SAMHD1, a dNTP hydrolase (dNTPase) and RNase, on HBV replication. We demonstrated that silencing of SAMHD1 in hepatic cells increased HBV replication, while overexpression had the opposite effect. SAMHD1 significantly affected the levels of extracellular viral DNA as well as intracellular reverse transcription products, without affecting HBV RNAs or cccDNA. SAMHD1 mutations that interfere with the dNTPase activity (D137N) or in the catalytic center of the histidine-aspartate (HD) domain (D311A), and a phospho-mimetic mutation (T592E), abrogated the inhibitory activity. In contrast, a mutation diminishing the potential RNase but not dNTPase activity (Q548A) and a mutation disabling phosphorylation (T592A) did not affect antiviral activity. Moreover, HBV restriction by SAMHD1 was rescued by addition of deoxynucleosides. Although HBV infection did not directly affect protein level or phosphorylation of SAMHD1, the virus upregulated intracellular dATPs. Interestingly, SAMHD1 was dephosphorylated, thus in a potentially antiviral-active state, in primary human hepatocytes. Furthermore, SAMHD1 was upregulated by type I and II interferons in hepatic cells. These results suggest that SAMHD1 is a relevant restriction factor for HBV and restricts reverse transcription through its dNTPase activity.
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