ArticlePLoS pathogens2018
A paralogous pair of mammalian host restriction factors form a critical host barrier against poxvirus infection.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 76 citations in OpenAlex.
- Structural mechanisms of SAMD9 autoinhibition and pathogenic dysregulation.Science advances · 2026Article
- Enhanced replication and immunogenicity of a genome-modified non-replicating vaccinia virus Tiantan strain for robust low-dose protection in mice.Journal of virology · 2026Article
- Lost in translation: interferon-stimulated genes targeting flavivirus protein synthesis.Journal of virology · 2026Review
- Evolutionary characterization of antiviral SAMD9/9L across kingdoms supports ancient convergence and lineage-specific adaptations.Nature ecology & evolution · 2025Article
- SAMD9L inhibits flavivirus translation independently of its capacity to trigger innate immune response.PLoS pathogens · 2025Article
- Mpox virus poxin-schlafen fusion protein suppresses innate antiviral response by sequestering STAT2.Emerging microbes & infections · 2025Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- Normal Immune Function in a Newborn With Early Identification of aClinical case reports · 2025Article
- Poly(A) tail dynamics, non-adenine incorporation and alternative polyadenylation shape the host transcriptome in COVID-19 pathogenesis.Scientific reports · 2025Article
- Poxvirus Host-Range Determinants: SAMD9/9L and Beyond.Annual review of virology · 2025Review
- Illuminating the mystery of thylacine extinction: a role for relaxed selection and gene loss.Proceedings. Biological sciences · 2025Article
- Structural and functional studies of rabbit SAMD9 reveal a distinct tRNase module that underlies the antiviral activity.PLoS pathogens · 2025Article
- Ancient convergence with prokaryote defense and recent adaptations to lentiviruses in primates characterize the ancestral immune factors SAMD9s.bioRxiv : the preprint server for biology · 2025Article
- SAMD9 senses cytosolic double-stranded nucleic acids in epithelial and mesenchymal cells to induce antiviral immunity.Nature communications · 2025Article
- Structural and Functional Studies of Rabbit SAMD9 Reveal a Distinct tRNase Module That Underlies the Antiviral Activity.bioRxiv : the preprint server for biology · 2025Article
- Temporal expression classes and functions of vaccinia virus and mpox (monkeypox) virus genes.mBio · 2025Review
- Review
- Abortive Infection of Animal Cells: What Goes Wrong.Annual review of virology · 2024Review
- SAMD9L acts as an antiviral factor against HIV-1 and primate lentiviruses by restricting viral and cellular translation.PLoS biology · 2024Article
- Malignant progression of preleukemic disorders.Blood · 2024Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Host restriction factors constitute a formidable barrier for viral replication to which many viruses have evolved counter-measures. Human SAMD9, a tumor suppressor and a restriction factor for poxviruses in cell lines, is antagonized by two classes of poxvirus proteins, represented by vaccinia virus (VACV) K1 and C7. A paralog of SAMD9, SAMD9L, is also encoded by some mammals, while only one of two paralogs is retained by others. Here, we show that SAMD9L functions similarly to SAMD9 as a restriction factor and that the two paralogs form a critical host barrier that poxviruses must overcome to establish infection. In mice, which naturally lack SAMD9, overcoming SAMD9L restriction with viral inhibitors is essential for poxvirus replication and pathogenesis. While a VACV deleted of both K1 and C7 (vK1L-C7L-) was restricted by mouse cells and highly attenuated in mice, its replication and virulence were completely restored in SAMD9L-/- mice. In humans, both SAMD9 and SAMD9L are poxvirus restriction factors, although the latter requires interferon induction in many cell types. While knockout of SAMD9 with Crispr-Cas9 was sufficient for abolishing the restriction for vK1L-C7L- in many human cells, knockout of both paralogs was required for abolishing the restriction in interferon-treated cells. Both paralogs are antagonized by VACV K1, C7 and C7 homologs from diverse mammalian poxviruses, but mouse SAMD9L is resistant to the C7 homolog encoded by a group of poxviruses with a narrow host range in ruminants, indicating that host species-specific difference in SAMD9/SAMD9L genes serves as a barrier for cross-species poxvirus transmission.
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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.