ArticleResearch in veterinary science2013
3C protein of feline coronavirus inhibits viral replication independently of the autophagy pathway.
Article in Research in veterinary science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed.
- Immune Cell Signaling in Feline Infectious Peritonitis Virus Infection and Implications for Vaccine Design.Vaccines · 2026Review
- Review
- Review
- Feline coronavirus with and without spike gene mutations detected by real-time RT-PCRs in cats with feline infectious peritonitis.Journal of feline medicine and surgery · 2020Article
- Review
- Mutation of the S and 3c genes in genomes of feline coronaviruses.The Journal of veterinary medical science · 2018Article
- Feline Coronaviruses: Pathogenesis of Feline Infectious Peritonitis.Advances in virus research · 2016Review
- Feline Coronavirus 3c Protein: A Candidate for a Virulence Marker?BioMed research international · 2016Article
- An update on feline infectious peritonitis: virology and immunopathogenesis.Veterinary journal (London, England : 1997) · 2014Review
- Identification and genotyping of feline infectious peritonitis-associated single nucleotide polymorphisms in the feline interferon-γ gene.Veterinary research · 2014Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Feline coronavirus (FCoV) can cause either asymptomatic enteric infection or fatal peritonitis in cats. Although the mutation of FCoV accessory gene 3c has been suggested to be related to the occurrence of feline infectious peritonitis (FIP), how the 3C protein is involved in this phenomenon remains unknown. To investigate the role of the 3C protein, a full-length 3c gene was transiently expressed and the cytoplasmic distribution of the protein was found to be primarily in the perinuclear region. Using 3c-stable expression cells, the replication of a 3c-defective FCoV strain was titrated and a significant decrease in replication (p<0.05) was observed. The mechanism underlying the decreased FIPV replication caused by the 3C protein was further investigated; neither the induction nor inhibition of autophagy rescued the viral replication. Taken together, our data suggest that the 3C protein might have a virulence-suppressing effect in FCoV-infected cats. Deletion of the 3c gene could therefore cause more efficient viral replication, which leads to a fatal 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.