ArticleFrontiers in microbiology2019
MYH9 Aggregation Induced by Direct Interaction With PRRSV GP5 Ectodomain Facilitates Viral Internalization by Permissive Cells.
Article in Frontiers in microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- The S32 amino acid deletion in the GP5 protein modulates the infectivity of porcine reproductive and respiratory syndrome virus.Virulence · 2026Article
- Elucidating the enigmatic biology of arteriviruses through receptor discovery.Journal of virology · 2026Review
- Numb-Associated Kinases-Mediated AP2M1 Activation Facilitates Porcine Reproductive and Respiratory Syndrome Virus Entry.Transboundary and emerging diseases · 2026Article
- A Porcine Monoclonal Antibody Targeting a Conserved GP4 Epitope Protects against In Vivo Infection via the Induction of Broad-Spectrum PRRSV Neutralization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Role of myosin heavy chain 9 in gastrointestinal tumorigenesis: A comprehensive review.World journal of gastrointestinal oncology · 2025Review
- Strategies and scheming: the war between PRRSV and host cells.Virology journal · 2025Review
- The neonatal Fc receptor (FcRn) is required for porcine reproductive and respiratory syndrome virus uncoating.Journal of virology · 2025Article
- Transcriptomic and Proteomic Analysis of Monkeypox Virus A5L-Expressing HEK293T Cells.International journal of molecular sciences · 2025Article
- Mechanism of PRRSV infection and antiviral role of polyphenols.Virulence · 2024Review
- Identification and biophysical characterization of epitope atlas of Porcine Reproductive and Respiratory Syndrome Virus.Computational and structural biotechnology journal · 2024Article
- Mass Spectrometry-Based Proteomic Analysis of Potential Host Proteins Interacting with GP5 in PRRSV-Infected PAMs.International journal of molecular sciences · 2024Article
- Research Progress on Glycoprotein 5 of Porcine Reproductive and Respiratory Syndrome Virus.Animals : an open access journal from MDPI · 2023Review
- Genetic background influences pig responses to porcine reproductive and respiratory syndrome virus.Frontiers in veterinary science · 2023Review
- A porcine reproductive and respiratory syndrome virus (PRRSV)-specific IgM as a novel adjuvant for an inactivated PRRSV vaccine improves protection efficiency and enhances cell-mediated immunity against heterologous PRRSV challenge.Veterinary research · 2022Article
- Research Progress in Porcine Reproductive and Respiratory Syndrome Virus-Host Protein Interactions.Animals : an open access journal from MDPI · 2022Review
- Review
- Identification of MYH9 Key Domain Involved in the Entry of PRRSV Into Permissive Cells.Frontiers in microbiology · 2022Article
- Reappraising host cellular factors involved in attachment and entry to develop antiviral strategies against porcine reproductive and respiratory syndrome virus.Frontiers in microbiology · 2022Review
- Combined Subcutaneous-Intranasal Immunization With Epitope-Based Antigens Elicits Binding and Neutralizing Antibody Responses in Serum and Mucosae Against PRRSV-2 and SARS-CoV-2.Frontiers in immunology · 2022Article
- Glyceraldehyde-3-Phosphate Dehydrogenase Restricted in Cytoplasmic Location by Viral GP5 Facilitates Porcine Reproductive and Respiratory Syndrome Virus Replication via Its Glycolytic Activity.Journal of virology · 2021Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prevention and control of infection by porcine reproductive and respiratory syndrome virus (PRRSV) remains a challenge, due to our limited understanding of the PRRSV invasion mechanism. Our previous study has shown that PRRSV glycoprotein GP5 interacts with MYH9 C-terminal domain protein (PRA). Here we defined that the first ectodomain of GP5 (GP5-ecto-1) directly interacted with PRA and this interaction triggered PRA and endogenous MYH9 to form filament assembly. More importantly, MYH9 filament assembly was also formed in GP5-ecto-1-transfected MARC-145 cells. Notably, PRRSV infection of MARC-145 cells and porcine alveolar macrophages also induced endogenous MYH9 aggregation and polymerization that were required for subsequent PRRSV internalization. Moreover, overexpression of S100A4, a MYH9-specific disassembly inducer, in MARC-145 cells significantly resulted in diminished MYH9 aggregation and marked inhibition of subsequent virion internalization and infection by both
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