ArticleProceedings of the National Academy of Sciences of the United States of America2007
Disruption of innate immunity due to mitochondrial targeting of a picornaviral protease precursor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 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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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.
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Who cites it
187 citing papers in PubMed, 314 citations in OpenAlex.
- Programmed to kill: AI-guided gasdermins eliminate virus-infected cells.Cell research · 2026Article
- Advances and perspectives in animal models of human hepatitis A virus.Animal models and experimental medicine · 2026Review
- Host species-specific mutations in the thumb domain of the 3Dpol polymerase are required for efficient replication of human hepatitis A virus in mice.PLoS pathogens · 2026Article
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- Natural killer cells and IFN-γ protect against liver injury during HAV infection in mice.Journal of virology · 2025Article
- The hepatitis E virus capsid protein ORF2 counteracts cell-intrinsic antiviral responses to enable persistent replication in cell culture.PLoS pathogens · 2025Article
- Heat shock protein 90 chaperone activity is required for hepatitis A virus replication.Journal of virology · 2025Article
- The structural protein VP3 of enterovirus D68 interacts with MAVS to inhibit the NF-κB signaling pathway.Journal of virology · 2025Article
- Redefining the immune landscape of hepatitis A virus infection.Experimental & molecular medicine · 2025Review
- Limited impact of hepatitis A virus 3C protease-mediated cleavage on the functions of NEMO in human hepatocytes.Journal of virology · 2025Article
- Identification of mutations in viral proteins involved in cell adaptation using a reverse genetic system of the live attenuated hepatitis A virus vaccine H2 strain.Virologica Sinica · 2024Article
- Use of virus-like particles and nanoparticle-based vaccines for combating picornavirus infections.Veterinary research · 2024Review
- Crosstalk between Dysfunctional Mitochondria and Proinflammatory Responses during Viral Infections.International journal of molecular sciences · 2024Review
- Natural-Target-Mimicking Translocation-Based Fluorescent Sensor for Detection of SARS-CoV-2 PLpro Protease Activity and Virus Infection in Living Cells.International journal of molecular sciences · 2024Article
- Identification and Genomic Characterization of Two Novel Hepatoviruses in Shrews from Yunnan Province, China.Viruses · 2024Article
- Respiratory Syncytial Virus Vaccine Design Using Structure-Based Machine-Learning Models.Viruses · 2024Article
- Article
- Picornavirus 3C Proteins Intervene in Host Cell Processes through Proteolysis and Interactions with RNA.Viruses · 2023Review
- Hepatitis A virus infection.Nature reviews. Disease primers · 2023Review
- Review
127 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial antiviral signaling protein (MAVS) is an essential component of virus-activated signaling pathways that induce protective IFN responses. Its localization to the outer mitochondrial membrane suggests an important yet unexplained role for mitochondria in innate immunity. Here, we show that hepatitis A virus (HAV), a hepatotropic picornavirus, ablates type 1 IFN responses by targeting the 3ABC precursor of its 3C(pro) cysteine protease to mitochondria where it colocalizes with and cleaves MAVS, thereby disrupting activation of IRF3 through the MDA5 pathway. The 3ABC cleavage of MAVS requires both the protease activity of 3C(pro) and a transmembrane domain in 3A that directs 3ABC to mitochondria. Lacking this domain, mature 3C(pro) protease is incapable of MAVS proteolysis. HAV thus disrupts host signaling by a mechanism that parallels that of the serine NS3/4A protease of hepatitis C virus, but differs in its use of a stable, catalytically active polyprotein processing intermediate. The unique requirement for mitochondrial localization of 3ABC underscores the importance of mitochondria to host control of virus infections within the liver.
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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.