ArticleJournal of virology2017
Replacement of Porcine CD163 Scavenger Receptor Cysteine-Rich Domain 5 with a CD163-Like Homolog Confers Resistance of Pigs to Genotype 1 but Not Genotype 2 Porcine Reproductive and Respiratory Syndrome Virus.
Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 120 citations in OpenAlex.
- Review
- CRISPR mediated PRRS resistant pigs: biological success, welfare implications, and ethical regulatory challenges for sustainable swine production.Porcine health management · 2026Review
- Signal peptide cleavage and ectodomain regions of GP2 are required for PRRSV infection.The Journal of general virology · 2026Article
- Elucidating the enigmatic biology of arteriviruses through receptor discovery.Journal of virology · 2026Review
- Knockout of SIGLEC1 in pigs reduces porcine reproductive and respiratory syndrome-1 (PRRSV-1) virus infection in primary macrophage cultures, but not in pigs.Virology journal · 2026Article
- Pigs with CD163 Mutation Conferred PRRSV Resistance.Animals : an open access journal from MDPI · 2026Article
- CD163 at the crossroads: a viral-exploited immunomodulator.Virology journal · 2026Review
- 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
- Application of CRISPR/Cas gene editing for infectious disease control in poultry.Open life sciences · 2025Review
- Mechanism of PRRSV infection and antiviral role of polyphenols.Virulence · 2024Review
- Linear epitopes of PRRSV-1 envelope proteins ectodomains are not correlated with broad neutralization.Porcine health management · 2024Article
- Review
- The neonatal Fc receptor (FcRn) is a pan-arterivirus receptor.Nature communications · 2024Article
- Genetically modified pigs with CD163 point mutation are resistant to HP-PRRSV infection.Zoological research · 2024Article
- A genome-wide CRISPR/Cas9 knockout screen identifies TMEM239 as an important host factor in facilitating African swine fever virus entry into early endosomes.PLoS pathogens · 2024Article
- Role of N-linked glycosylation in porcine reproductive and respiratory syndrome virus (PRRSV) infection.The Journal of general virology · 2024Article
- Single amino acid mutation of nectin-1 provides remarkable resistance against lethal pseudorabies virus infection in mice.The Journal of veterinary medical science · 2024Article
- Pigs lacking the SRCR5 domain of CD163 protein demonstrate heritable resistance to the PRRS virus and no changes in animal performance from birth to maturity.Frontiers in genome editing · 2024Article
- Porcine Reproductive and Respiratory Syndrome (PRRS) andAnimals : an open access journal from MDPI · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD163 knockout (KO) pigs are resistant to infection with genotype 2 (type 2) porcine reproductive and respiratory syndrome virus (PRRSV). Furthermore, the substitution of CD163 scavenger receptor cysteine-rich (SRCR) domain 5 with a homolog of human CD163-like (hCD163L1) SRCR 8 domain confers resistance of transfected HEK cells to type 1 PRRSV. As a means to understand the role of domain 5 in PRRSV infection with both type 1 and type 2 viruses, pigs were genetically modified (GM) to possess one of the following genotypes: complete knockout (KO) of CD163, deletions within SRCR domain 5, or replacement (domain swap) of SRCR domain 5 with a synthesized exon encoding a homolog of hCD163L1 SRCR domain 8. Immunophenotyping of porcine alveolar macrophages (PAMs) showed that pigs with the KO or SRCR domain 5 deletion did not express CD163. When placed in culture, PAMs from pigs with the CD163 KO phenotype were completely resistant to a panel consisting of six type 1 and nine type 2 isolates. PAMs from pigs that possessed the hCD163L1 domain 8 homolog expressed CD163 and supported the replication of all type 2 isolates, but no type 1 viruses. Infection of CD163-modified pigs with representative type 1 and type 2 viruses confirmed the in vitro results. The results confirm that CD163 is the likely receptor for all PRRS viruses. Even though type 1 and type 2 viruses are considered phenotypically similar at several levels, there is a distinct difference between the viral genotypes in the recognition of CD163. IMPORTANCE: Genetic modification of the CD163 gene creates the opportunity to develop production animals that are resistant to PRRS, the costliest viral disease to ever face the swine industry. The results create further opportunities to develop refinements in the modification of CD163 with the goal of making pigs refractory to infection while retaining important CD163 functions.
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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.