ArticleProceedings of the National Academy of Sciences of the United States of America2017
Triad of human cellular proteins, IRF2, FAM111A, and RFC3, restrict replication of orthopoxvirus SPI-1 host-range mutants.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Expanding the Phenotypic Spectrum of Kenny-Caffey Syndrome.The Journal of clinical endocrinology and metabolism · 2023Pooled it
- Distinct ATRX functions cooperate with 9-1-1 and CST complexes to safeguard replication and telomere integrity.Nature structural & molecular biology · 2026Article
- Diversity of fecal viromes and zoonotic risk assessment in captive wild felids using viral metagenomics.Scientific reports · 2026Article
- The FAM111A Gene: Genetic, Epigenetic, and Pharmacological Targets and Mechanistic Insights with Clinical Relevance.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Poxvirus Host-Range Determinants: SAMD9/9L and Beyond.Annual review of virology · 2025Review
- Regulation of viral replication by host restriction factors.Frontiers in immunology · 2025Review
- Kenny-Caffey Syndrome Type 2 (KCS2): A New Case Report and Patient Follow-Up Optimization.Journal of clinical medicine · 2024Article
- E2F3-dependent activation of FAM111B restricts mouse cytomegalovirus replication in primate cells.Journal of virology · 2024Article
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- Abortive Infection of Animal Cells: What Goes Wrong.Annual review of virology · 2024Review
- Dimerization-dependent serine protease activity of FAM111A prevents replication fork stalling at topoisomerase 1 cleavage complexes.Nature communications · 2024Article
- Unravelling the Intricate Roles of FAM111A and FAM111B: From Protease-Mediated Cellular Processes to Disease Implications.International journal of molecular sciences · 2024Review
- Quantitative proteomics defines mechanisms of antiviral defence and cell death during modified vaccinia Ankara infection.Nature communications · 2023Article
- Human FAM111A inhibits vaccinia virus replication by degrading viral protein I3 and is antagonized by poxvirus host range factor SPI-1.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Gene-nutrient interactions that impact magnesium homeostasis increase risk for neural tube defects in mice exposed to dolutegravir.Frontiers in cell and developmental biology · 2023Article
- FAM111A is dispensable for electrolyte homeostasis in mice.Scientific reports · 2022Article
- Functions and evolution of FAM111 serine proteases.Frontiers in molecular biosciences · 2022Review
- IRF2 inhibits ZIKV replication by promoting FAM111A expression to enhance the host restriction effect of RFC3.Virology journal · 2021Article
- Differential Regulation of Cellular FAM111B by Human Adenovirus C Type 5 E1 Oncogenes.Viruses · 2021Article
- FAM111A induces nuclear dysfunction in disease and viral restriction.EMBO reports · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Viruses and their hosts can reach balanced states of evolution ensuring mutual survival, which makes it difficult to appreciate the underlying dynamics. To uncover hidden interactions, virus mutants that have lost defense genes may be used. Deletion of the gene that encodes serine protease inhibitor 1 (SPI-1) of rabbitpox virus and vaccinia virus, two closely related orthopoxviruses, prevents their efficient replication in human cells, whereas certain other mammalian cells remain fully permissive. Our high-throughput genome-wide siRNA screen identified host factors that prevent reproduction and spread of the mutant viruses in human cells. More than 20,000 genes were interrogated with individual siRNAs and those that prominently increased replication of the SPI-1 deletion mutant were subjected to a secondary screen. The top hits based on the combined data-replication factor C3 (RFC3), FAM111A, and interferon regulatory factor 2 (IRF2)-were confirmed by custom assays. The siRNAs to RFC1, RFC2, RFC4, and RFC5 mRNAs also enhanced spread of the mutant virus, strengthening the biological significance of the RFC complex as a host restriction factor for poxviruses. Whereas association with proliferating cell nuclear antigen and participation in processive genome replication are common features of FAM111A and RFC, IRF2 is a transcriptional regulator. Microarray analysis, quantitative RT-PCR, and immunoblotting revealed that IRF2 regulated the basal level expression of FAM111A, suggesting that the enhancing effect of depleting IRF2 on replication of the SPI-1 mutant was indirect. Thus, the viral SPI-1 protein and the host IRF2, FAM111A, and RFC complex likely form an interaction network that influences the ability of poxviruses to replicate in human cells.
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