ArticleJournal of virology2005
Amino acid changes in proteins 2B and 3A mediate rhinovirus type 39 growth in mouse cells.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Human Stimulator of Interferon Genes Promotes Rhinovirus C Replication in Mouse Cells In Vitro and In Vivo.Viruses · 2024Article
- Directed Evolution of Seneca Valley Virus in Tumorsphere and Monolayer Cell Cultures of a Small-Cell Lung Cancer Model.Cancers · 2023Article
- Picornaviruses: A View from 3A.Viruses · 2021Review
- Biological Function and Application of Picornaviral 2B Protein: A New Target for Antiviral Drug Development.Viruses · 2019Review
- Foot-and-Mouth Disease Virus Antagonizes NOD2-Mediated Antiviral Effects by Inhibiting NOD2 Protein Expression.Journal of virology · 2019Article
- A Single Point Mutation in the Rhinovirus 2B Protein Reduces the Requirement for Phosphatidylinositol 4-Kinase Class III Beta in Viral Replication.Journal of virology · 2018Article
- Human Rhinovirus Diversity and Evolution: How Strange the Change from Major to Minor.Journal of virology · 2017Article
- Foot-and-Mouth Disease Virus Viroporin 2B Antagonizes RIG-I-Mediated Antiviral Effects by Inhibition of Its Protein Expression.Journal of virology · 2016Article
- Mutations in VP1 and 3A proteins improve binding and replication of rhinovirus C15 in HeLa-E8 cells.Virology · 2016Article
- Biological function of Foot-and-mouth disease virus non-structural proteins and non-coding elements.Virology journal · 2016Review
- Temperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Reverse genetics system for studying human rhinovirus infections.Methods in molecular biology (Clifton, N.J.) · 2015Article
- Development of a reverse-genetics system for murine norovirus 3: long-term persistence occurs in the caecum and colon.The Journal of general virology · 2012Article
- Selection of rhinovirus 1A variants adapted for growth in mouse lung epithelial cells.Virology · 2011Article
- A host-specific, temperature-sensitive translation defect determines the attenuation phenotype of a human rhinovirus/poliovirus chimera, PV1(RIPO).Journal of virology · 2011Article
- Adaptation of an ICAM-1-tropic enterovirus to the mouse respiratory tract.Journal of virology · 2011Article
- Article
- The human rhinovirus: human-pathological impact, mechanisms of antirhinoviral agents, and strategies for their discovery.Medicinal research reviews · 2011Review
- A mutant of infectious Asia 1 serotype foot-and-mouth disease virus with the deletion of 10-amino-acid in the 3A protein.Virus genes · 2010Article
- Animal models of virus-induced chronic airway disease.Immunology and allergy clinics of North America · 2010Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Many steps of viral replication are dependent on the interaction of viral proteins with host cell components. To identify rhinovirus proteins involved in such interactions, human rhinovirus 39 (HRV39), a virus unable to replicate in mouse cells, was adapted to efficient growth in mouse cells producing the viral receptor ICAM-1 (ICAM-L cells). Amino acid changes were identified in the 2B and 3A proteins of the adapted virus, RV39/L. Changes in 2B were sufficient to permit viral growth in mouse cells; however, changes in both 2B and 3A were required for maximal viral RNA synthesis in mouse cells. Examination of infected HeLa cells by electron microscopy demonstrated that human rhinoviruses induced the formation of cytoplasmic membranous vesicles, similar to those observed in cells infected with other picornaviruses. Vesicles were also observed in the cytoplasm of HRV39-infected mouse cells despite the absence of viral RNA replication. Synthesis of picornaviral nonstructural proteins 2C, 2BC, and 3A is known to be required for formation of membranous vesicles. We suggest that productive HRV39 infection is blocked in ICAM-L cells at a step posttranslation and prior to the formation of a functional replication complex. The observation that changes in HRV39 2B and 3A proteins lead to viral growth in mouse cells suggests that one or both of these proteins interact with host cell proteins to promote viral replication.
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