ArticleJournal of virology2021
Inducible Guanylate-Binding Protein 7 Facilitates Influenza A Virus Replication by Suppressing Innate Immunity via NF-κB and JAK-STAT Signaling Pathways.
Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Tissue and cellular spatiotemporal dynamics in colon aging.Nature biotechnology · 2026Article
- Long-term isolation and archaic introgression shape functional genetic variation in Near Oceania.Science (New York, N.Y.) · 2026Article
- Post-translational modification networks as master regulators of influenza virus replication, host adaptation, and immune evasion.Frontiers in immunology · 2026Review
- Local and systemic host responses to influenza and concurrent or sequential SARS-CoV-2 infection.Frontiers in cellular and infection microbiology · 2026Review
- Proteomic Changes in the Cytoplasmatic Fraction of Weaned Piglets' Liver and Kidney Under Antioxidant and Mycotoxin Diets.Antioxidants (Basel, Switzerland) · 2025Article
- Guanylate binding proteins (GBPs) as novel therapeutic targets against single-stranded RNA viruses.Molecular biology reports · 2025Review
- Functional Involvement of Signal Transducers and Activators of Transcription in the Pathogenesis of Influenza A Virus.International journal of molecular sciences · 2024Review
- Gene expression profile analysis of severe influenza-based modulation of idiopathic pulmonary fibrosis.European journal of medical research · 2024Article
- Article
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- Guanylate-binding protein 1 acts as a pro-viral factor for the life cycle of hepatitis C virus.PLoS pathogens · 2024Article
- Amino acid 138 in the HA of a H3N2 subtype influenza A virus increases affinity for the lower respiratory tract and alveolar macrophages in pigs.PLoS pathogens · 2024Article
- Virus versus host: influenza A virus circumvents the immune responses.Frontiers in microbiology · 2024Review
- Article
- Functional cross-species conservation of guanylate-binding proteins in innate immunity.Medical microbiology and immunology · 2023Review
- Nisoldipine Inhibits Influenza A Virus Infection by Interfering with Virus Internalization Process.Viruses · 2022Article
- Article
- Human Guanylate-Binding Protein 1 Positively Regulates Japanese Encephalitis Virus Replication in an Interferon Gamma Primed Environment.Frontiers in cellular and infection microbiology · 2022Article
- Differentially Expressed Gene Patterns in Ascarid-Infected Chickens of Higher- or Lower-Performing Genotypes.Animals : an open access journal from MDPI · 2021Article
- Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Guanylate-binding protein 7 (GBP7) belongs to the GBP family, which plays key roles in mediating innate immune responses to intracellular pathogens. Thus far, GBP7 has been reported to be a critical cellular factor against bacterial infection. However, the relationship between GBP7 and influenza A virus (IAV) replication is unknown. Here, we showed that GBP7 expression was significantly upregulated in the lungs of mice, human peripheral blood mononuclear cells (PBMCs), and A549 cells during IAV infection. Using the CRISPR-Cas9 system and overexpression approaches, it was found that GBP7 knockout inhibited IAV replication by enhancing the expression of IAV-induced type I interferon (IFN), type III IFN, and proinflammatory cytokines. Conversely, overexpression of GBP7 facilitated IAV replication by suppressing the expression of those factors. Furthermore, GBP7 knockout enhanced IAV-induced nuclear factor-κB (NF-κB) activation and phosphorylation of stat1 and stat2; overexpression of GBP7 had the opposite effect. Our data indicated that GBP7 suppresses innate immune responses to IAV infection via NF-κB and JAK-STAT signaling pathways. Taken together, upon IAV infection, the induced GBP7 facilitated IAV replication by suppressing innate immune responses to IAV infection, which suggested that GBP7 serves as a therapeutic target for controlling IAV infection.
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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.