ArticleViruses2022
A Single Amino Acid Substitution in Porcine Reproductive and Respiratory Syndrome Virus Glycoprotein 2 Significantly Impairs Its Infectivity in Macrophages.
Article in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Signal peptide cleavage and ectodomain regions of GP2 are required for PRRSV infection.The Journal of general virology · 2026Article
- In Vitro Characterization of Vaccine Strain-like Porcine Reproductive and Respiratory Syndrome Virus Strains Isolated from Weaned Pigs Exhibiting Respiratory Symptoms.Pathogens (Basel, Switzerland) · 2025Article
- GP2a I118 and GP4 D43 play critical roles in the attachment of PRRSV to the CD163 receptor: implications for anti-PRRSV infection targets.Journal of virology · 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 GP2a 91/97/98 amino acid substitutions play critical roles in determining PRRSV tropism and infectivity but do not affect immune responses.Journal of virology · 2025Article
- New insights into the testicular tropism of porcine reproductive and respiratory syndrome virus.Microbiology spectrum · 2025Article
- Article
- Reverse genetics construction and pathogenicity of a novel recombinant NADC30-like PRRSV isolated in China.Frontiers in veterinary science · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) has a restricted tropism for macrophages and CD163 is a key receptor for infection. In this study, the PRRSV strain NCV1 was passaged on MARC-145 cells for 95 passages, and two plaque-clones (C1 and C2) were randomly selected for further analysis. The C1 virus nearly lost the ability to infect porcine alveolar macrophages (PAMs), as well as porcine kidney cells expressing porcine CD163 (PK15-pCD163), while the C2 virus replicates well in these two cell types. Pretreatment of MARC-145 cells with an anti-CD163 antibody nearly blocked C1 virus infection, indicating that the virus still required CD163 to infect cells. The C1 virus carried four unique amino acid substitutions: three in the nonstructural proteins and a K160I in GP2. The introduction of an I160K substitution in GP2 of the C1 virus restored its infectivity in PAMs and PK15-pCD163 cells, while the introduction of a K160I substitution in GP2 of the low-passaged, virulent PRRSV strain NCV13 significantly impaired its infectivity. Importantly, pigs inoculated with the rNCV13-K160I mutant exhibited lower viremia levels and lung lesions than those infected with the parental rNCV13. These results demonstrated that the K160 residue in GP2 is one of the key determinants of PRRSV tropism.
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