ArticleJournal of virology2022
Genome-Wide CRISPR/Cas9 Screen Reveals a Role for SLC35A1 in the Adsorption of Porcine Deltacoronavirus.
Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
- The essential role of heparan sulfate in the entry of PDCoV and other porcine coronaviruses.Virulence · 2026Article
- Monoclonal antibodies target conserved S1mBio · 2026Article
- PRMT3 restricts porcine epidemic diarrhea virus replication by disrupting the interaction between VAPA and the viral nucleocapsid protein.PLoS pathogens · 2026Article
- Identification of TMEM41B TM6 as a critical domain for coronavirus replicationJournal of virology · 2026Article
- PEX19 restricts porcine deltacoronavirus replication through farnesylation-dependent and -independent mechanisms.Journal of virology · 2026Article
- Genome-wide CRISPR/Cas9 knockout screen identifies host factors essential for bovine parainfluenza virus type 3 replication.Science China. Life sciences · 2026Article
- Cell entry mechanisms of porcine enteric coronaviruses.The Journal of biological chemistry · 2026Review
- CRISPR-based screening of host factors in veterinary viral infections: from target discovery to host-directed antiviral strategies.Frontiers in veterinary science · 2026Review
- Pig Genome Editing for Agriculture: Achievements and Challenges.International journal of molecular sciences · 2025Review
- A comprehensive PDCoV-host proteome interaction map reveals potential antiviral targets.PLoS pathogens · 2025Article
- Article
- Membrane protein CRISPR screen identifies RPSA as an essential host factor for porcine epidemic diarrhea virus replication.Journal of virology · 2025Article
- IFITM proteins are key entry factors for porcine epidemic diarrhea coronavirus.Journal of virology · 2025Article
- Molecular breeding of pigs in the genome editing era.Genetics, selection, evolution : GSE · 2025Review
- Gene Editing for Enhanced Swine Production: Current Advances and Prospects.Animals : an open access journal from MDPI · 2025Review
- Swine Acute Diarrhea Syndrome Coronavirus: An Overview of Virus Structure and Virus-Host Interactions.Animals : an open access journal from MDPI · 2025Review
- SLC35A2 gene product modulates paramyxovirus fusion events during infection.PLoS pathogens · 2025Article
- CRISPR-Mediated Library Screening of Gene-Knockout Cell Lines for Investigating Antiviral Innate Immunity.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Genome-wide CRISPR/Cas9 library screen identifies C16orf62 as a host dependency factor for porcine deltacoronavirus infection.Emerging microbes & infections · 2024Article
- Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine deltacoronavirus (PDCoV), an emerging enteropathogenic coronavirus, not only causes diarrhea in piglets but also possesses the potential to infect humans. To better understand host-virus genetic dependencies and find potential therapeutic targets for PDCoV, we used a porcine single-guide RNA (sgRNA) lentivirus library to screen host factors related to PDCoV infection in LLC-PK1 cells. The solute carrier family 35 member A1 (SLC35A1), a key molecule in the sialic acid (SA) synthesis pathway, was identified as a host factor required for PDCoV infection. A knockout of SLC35A1 caused decreases in the amounts of cell surface sialic acid (SA) and viral adsorption; meanwhile, trypsin promoted the use of SA in PDCoV infection. By constructing and assessing a series of recombinant PDCoV strains with the deletion or mutation of possible critical domain or amino acid residues for SA binding in the S1 N-terminal domain, we found that S T182 might be a PDCoV SA-binding site. However, the double knockout of SLC35A1 and amino peptidase N (APN) could not block PDCoV infection completely. Additionally, we found that different swine enteric coronaviruses, including transmissible gastroenteritis coronavirus, porcine epidemic diarrhea virus, and swine acute diarrhea syndrome coronavirus, are differentially dependent on SA. Overall, our study uncovered a collection of host factors that can be exploited as drug targets against PDCoV infection and deepened our understanding of the relationship between PDCoV and SA.
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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.