ArticleJournal of virology2007
Human rhinovirus type 54 infection via heparan sulfate is less efficient and strictly dependent on low endosomal pH.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 37 citations in OpenAlex.
- Open questions in enterovirus uncoating.Journal of virology · 2026Review
- Pathogens that infect mammalian cells via sulfonated glycosaminoglycans.Frontiers in cellular and infection microbiology · 2025Review
- Heparin, Low Molecular Weight Heparin, and Non-Anticoagulant Derivatives for the Treatment of Inflammatory Lung Disease.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Orosomucoid-like protein 3, rhinovirus and asthma.World journal of critical care medicine · 2021Review
- Structural Insight into Non-Enveloped Virus Binding to Glycosaminoglycan Receptors: A Review.Viruses · 2021Review
- Polyamine Depletion Abrogates Enterovirus Cellular Attachment.Journal of virology · 2019Article
- Heparan Sulfate Proteoglycans and Viral Attachment: True Receptors or Adaptation Bias?Viruses · 2019Review
- Coxsackievirus A16 utilizes cell surface heparan sulfate glycosaminoglycans as its attachment receptor.Emerging microbes & infections · 2017Article
- Mutations in VP1 and 3A proteins improve binding and replication of rhinovirus C15 in HeLa-E8 cells.Virology · 2016Article
- Viral entry pathways: the example of common cold viruses.Wiener medizinische Wochenschrift (1946) · 2016Review
- Rhinoviruses and Their Receptors: Implications for Allergic Disease.Current allergy and asthma reports · 2016Review
- Role of Heparan Sulfate in Cellular Infection of Integrin-Binding Coxsackievirus A9 and Human Parechovirus 1 Isolates.PloS one · 2016Article
- Symmetry-related clustering of positive charges is a common mechanism for heparan sulfate binding in enteroviruses.Journal of virology · 2012Article
- Viral quasispecies evolution.Microbiology and molecular biology reviews : MMBR · 2012Review
- Clinical and molecular features of human rhinovirus C.Microbes and infection · 2012Review
- Insights into minor group rhinovirus uncoating: the X-ray structure of the HRV2 empty capsid.PLoS pathogens · 2012Article
- Productive entry pathways of human rhinoviruses.Advances in virology · 2012Article
- The human rhinovirus: human-pathological impact, mechanisms of antirhinoviral agents, and strategies for their discovery.Medicinal research reviews · 2011Review
- Human rhinovirus 14 enters rhabdomyosarcoma cells expressing icam-1 by a clathrin-, caveolin-, and flotillin-independent pathway.Journal of virology · 2010Article
- Low pH-triggered beta-propeller switch of the low-density lipoprotein receptor assists rhinovirus infection.Journal of virology · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
K-type major-group human rhinoviruses (HRVs) (including HRV54) share a prominent lysine residue in the HI surface loop of VP1 with all minor-group HRVs. Despite the presence of this residue, they cannot use members of the low-density lipoprotein receptor family for productive infection. Reexamining all K-type viruses for receptor usage, we noticed that HRV54 is able to replicate in RD cells that lack the major-group receptor intercellular adhesion molecule 1 (ICAM-1). By using receptor blocking assays, inhibition of sulfation, enzymatic digestion, and proteoglycan-deficient cell lines, we show here that wild-type HRV54, without any adaptation, uses heparan sulfate (HS) proteoglycan as an alternate receptor. However, infection via HS is less efficient than infection via ICAM-1. Moreover, HRV54 has an acid lability profile similar to that of the minor-group virus HRV2. In ICAM-1-deficient cells its replication is completely blocked by the H(+)-ATPase inhibitor bafilomycin A1, whereas in ICAM-1-expressing cells it replicates in the presence of the drug. Thus, use of a "noncatalytic" receptor requires the virus to be highly unstable at low pH.
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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.