ArticleOncotarget2018
Porcine alveolar macrophage CD163 abundance is a pivotal switch for porcine reproductive and respiratory syndrome virus infection.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed, 49 citations in OpenAlex.
- CD163 at the crossroads: a viral-exploited immunomodulator.Virology journal · 2026Review
- Advances in the immunosuppression of porcine reproductive and respiratory syndrome virus.Frontiers in veterinary science · 2026Review
- Numb-Associated Kinases-Mediated AP2M1 Activation Facilitates Porcine Reproductive and Respiratory Syndrome Virus Entry.Transboundary and emerging diseases · 2026Article
- Article
- Galectin 3-binding protein suppresses PRRSV replication via Cullin3-mediated ubiquitination degradation of non-structural protein 12.Journal of virology · 2025Article
- Alpha-herpesvirus US1 interacts with cGAS to suppress type I IFN responses and antiviral defense.PLoS pathogens · 2025Article
- Nsp2 replicase-mediated viral uncoating in porcine alveolar macrophages contributes to the attenuation of PRRSV-2 live attenuated vaccine.Journal of virology · 2025Article
- The neonatal Fc receptor (FcRn): Guardian or Trojan Horse in viral infection?PLoS pathogens · 2025Review
- The full-length nsp2 replicase contributes to viral assembly in highly pathogenic PRRSV-2.Journal of virology · 2025Article
- Development of a Competitive ELISA for Detecting Antibodies Against Pseudorabies Virus Glycoprotein D.Transboundary and emerging diseases · 2025Article
- Article
- Species-specific IL-1β is an inflammatory sensor of Seneca Valley Virus 3C Protease.PLoS pathogens · 2024Article
- Innate Immune Evasion of PRRSV nsp11 through Degradation of the HDAC2 by Its Endoribonuclease Activity.Viruses · 2024Article
- Lactate-lactylation-HSPA6 axis promotes PRRSV replication by impairing IFN-β production.Journal of virology · 2024Article
- Generation of an infectious cDNA clone for NADC30-like PRRSV.Frontiers in veterinary science · 2024Article
- Minor envelope proteins from GP2a to GP4 contribute to the spread pattern and yield of type 2 PRRSV in MARC-145 cells.Frontiers in cellular and infection microbiology · 2024Article
- Recombinant characteristics and pathogenicity of a novel PRRSV variant in weaned piglets derived from recombination of three clinical epidemic strains.Frontiers in veterinary science · 2024Article
- Glycoprotein Non-Metastatic Melanoma Protein B Restricts PRRSV Replication by Inhibiting Autophagosome-Lysosome Fusion.Viruses · 2023Article
- Interaction between Porcine Alveolar Macrophage-Tang Cells and Streptococcus suis Strains of Different Virulence: Phagocytosis and ApoptosisMicroorganisms · 2023Article
- TurboID Screening of the OmpP2 Protein Reveals Host Proteins Involved in Recognition and Phagocytosis ofMicrobiology spectrum · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) is a problematic virus that is difficult to control. The principal target cells for PRRSV infection are porcine alveolar macrophages (PAMs). Increasing evidence has demonstrated that CD163 is the determinant receptor for PRRSV infection. However, the relationship between CD163 abundance and PRRSV infection is unclear. In this study, we first generated primary immortalized PAMs (iPAMs) using SV40 large T antigen and demonstrated that CD163 expression is suppressed by the alternative splicing of mRNA in iPAMs. Two forms of CD163 transcripts were discovered, and most iPAMs expressed a short-form CD163 transcript that lacked from scavenger receptor cysteine-rich tandem repeat 1 (SRCR1) to SRCR5 of the functional domain. More importantly, using flow cytometric cell sorting technology, we isolated CD163-positive single-cell-derived clones with varying CD163 abundances to investigate the relationship between CD163 abundance and PRRSV infection. For the first time, we showed that cells with low CD163 abundance (approximately 20%) do not initiate PRRSV infection, while cells with moderate CD163 abundance display limited infection. PRRSV initiated efficient infection only in cells with high CD163 abundances. Our results demonstrate that CD163 abundance is a pivotal switch for PRRSV replication.
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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.