ArticleJournal of virology2009
Vaccinia virus K1L and C7L inhibit antiviral activities induced by type I interferons.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 69 citations in OpenAlex.
- 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
- Poxvirus Host-Range Determinants: SAMD9/9L and Beyond.Annual review of virology · 2025Review
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- Understanding the performance of HIV-1 viral vector vaccines: adenovirus and poxvirus case studies.Frontiers in immunology · 2025Review
- Molecular Evolution of Protein Sequences and Codon Usage in Monkeypox Viruses.Genomics, proteomics & bioinformatics · 2024Article
- Review
- Human SAMD9 is a poxvirus-activatable anticodon nuclease inhibiting codon-specific protein synthesis.Science advances · 2023Article
- Comprehensive literature review of monkeypox.Emerging microbes & infections · 2022Review
- The employment of vaccinia virus for colorectal cancer treatment: A review of preclinical and clinical studies.Human vaccines & immunotherapeutics · 2022Review
- Structure and function of an effector domain in antiviral factors and tumor suppressors SAMD9 and SAMD9L.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Identification of protective T-cell antigens for smallpox vaccines.Cytotherapy · 2020Article
- Buffalopox Virus: An Emerging Virus in Livestock and Humans.Pathogens (Basel, Switzerland) · 2020Review
- Rescue of a Vaccinia Virus Mutant Lacking IFN Resistance Genes K1L and C7L by theFrontiers in microbiology · 2020Article
- mTOR Dysregulation by Vaccinia Virus F17 Controls Multiple Processes with Varying Roles in Infection.Journal of virology · 2019Article
- Identification of CP77 as the Third Orthopoxvirus SAMD9 and SAMD9L Inhibitor with Unique Specificity for a Rodent SAMD9L.Journal of virology · 2019Article
- Translational control during poxvirus infection.Wiley interdisciplinary reviews. RNA · 2019Review
- Article
- Vaccinia virus-mediated cancer immunotherapy: cancer vaccines and oncolytics.Journal for immunotherapy of cancer · 2019Review
- Human Host Range Restriction of the Vaccinia Virus C7/K1 Double Deletion Mutant Is Mediated by an Atypical Mode of Translation Inhibition.Journal of virology · 2018Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Cellular tropism of vaccinia virus (VACV) is regulated by host range genes, including K1L, C7L, and E3L. While E3L is known to support viral replication by antagonizing interferon (IFN) effectors, including PKR, the exact functions of K1L and C7L are unclear. Here, we show that K1L and C7L can also inhibit antiviral effectors induced by type I IFN. In human Huh7 and MCF-7 cells, a VACV mutant lacking both K1L and C7L (vK1L-C7L-) replicated as efficiently as wild-type (WT) VACV, even in the presence of IFN. However, pretreating the cells with type I IFN, while having very little effect on WT VACV, blocked the replication of vK1L-C7L- at the step of intermediate viral gene translation. Restoring either K1L or C7L to vK1L(-)C7L(-) fully restored the IFN resistance phenotype. The deletion of K1L and C7L from VACV did not affect the ability of the virus to inhibit IFN signaling or its ability to inhibit the phosphorylation of PKR and the alpha subunit of eukaryotic initiation factor 2, indicating that K1L and C7L function by antagonizing an IFN effector(s) but with a mechanism that is different from those of IFN antagonists previously identified for VACV. Mutations of K1L that inactivate the host range function also rendered K1L unable to antagonize IFN, suggesting that K1L supports VACV replication in mammalian cells by antagonizing the same antiviral factor(s) that is induced by IFN in Huh7 cells.
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What OpenQuestion holds
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.