ArticleJournal of virology2003
Alteration of hepatitis A virus (HAV) particles by a soluble form of HAV cellular receptor 1 containing the immunoglobin-and mucin-like regions.
Article in Journal of virology, 2003. 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 70 citations in OpenAlex.
- The Role of Viral Infections in Acute Kidney Injury and Mesenchymal Stem Cell-Based Therapy.Stem cell reviews and reports · 2025Review
- Molecular Basis for the Differential Function of HAVCR1 Mucin Variants.Biomedicines · 2024Article
- SARS-CoV-2 Omicron: Viral Evolution, Immune Evasion, and Alternative Durable Therapeutic Strategies.Viruses · 2024Review
- An ACE2 decamer viral trap as a durable intervention solution for current and future SARS-CoV.Emerging microbes & infections · 2023Article
- Oligomers of hepatitis A virus (HAV) capsid protein VP1 generated in a heterologous expression system.Microbial cell factories · 2022Article
- Reply to Das et al., "TIM1 (HAVCR1): an Essential 'Receptor' or an 'Accessory Attachment Factor' for Hepatitis A Virus?"Journal of virology · 2019Article
- Understanding kidney injury molecule 1: a novel immune factor in kidney pathophysiology.American journal of translational research · 2019Review
- HAVCR1 (CD365) and Its Mouse Ortholog Are Functional Hepatitis A Virus (HAV) Cellular Receptors That Mediate HAV Infection.Journal of virology · 2018Article
- Potent neutralization of hepatitis A virus reveals a receptor mimic mechanism and the receptor recognition site.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- The Coxsackievirus and Adenovirus Receptor: Glycosylation and the Extracellular D2 Domain Are Not Required for Coxsackievirus B3 Infection.Journal of virology · 2016Article
- TIM-1 acts a dual-attachment receptor for Ebolavirus by interacting directly with viral GP and the PS on the viral envelope.Protein & cell · 2015Article
- The VP4 peptide of hepatitis A virus ruptures membranes through formation of discrete pores.Journal of virology · 2014Article
- Molecular biology and inhibitors of hepatitis A virus.Medicinal research reviews · 2014Review
- Defect in regulatory B-cell function and development of systemic autoimmunity in T-cell Ig mucin 1 (Tim-1) mucin domain-mutant mice.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Tim-1 regulates Th2 responses in an airway hypersensitivity model.European journal of immunology · 2012Article
- A polymorphism in TIM1 is associated with susceptibility to severe hepatitis A virus infection in humans.The Journal of clinical investigation · 2011Article
- Determinants in 3Dpol modulate the rate of growth of hepatitis A virus.Journal of virology · 2010Article
- Increased expression of human T-cell immunoglobulin- and mucin-domain-containing molecule-4 in peripheral blood mononuclear cells from patients with system lupus erythematosus.Cellular & molecular immunology · 2010Article
- Picornaviruses.Current topics in microbiology and immunology · 2010Article
- The interaction of hepatitis A virus (HAV) with soluble forms of its cellular receptor 1 (HAVCR1) share the physiological requirements of infectivity in cell culture.Virology journal · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis A virus (HAV) infects African green monkey kidney cells via HAV cellular receptor 1 (havcr-1). The ectodomain of havcr-1 contains an N-terminal cysteine-rich immunoglobin-like region (D1), followed by a mucin-like region that extends D1 well above the cell surface. D1 is required for binding of HAV, and a soluble construct containing D1 fused to the hinge and Fc portions of human immunoglobin G1 (IgG1), D1-Fc, bound and neutralized HAV inefficiently. However, D1-Fc did not alter the virions. To determine whether additional regions of havcr-1 are required to trigger uncoating of HAV, we constructed D1muc-Fc containing D1 and two-thirds of the mucin-like region fused to the Fc and hinge portions of human IgG1. D1muc-Fc neutralized 10 times more HAV than did D1-Fc. Sedimentation analysis in sucrose gradients showed that treatment of HAV with 20 to 200 nM D1muc-Fc disrupted the majority of the virions, whereas treatment with 2 nM D1muc-Fc had no effect on the sedimentation of the particles. Treatment of HAV with 100 nM D1muc-Fc resulted in low-level accumulation of 100- to 125S particles. Negative-stain electron microscopy analysis revealed that the 100- to 125S particles had the characteristics of disrupted virions, such as internal staining and diffuse edges. Quantitative PCR analysis showed that the 100- to 125S particles contained viral RNA. These results indicate that D1 and the mucin-like region of havcr-1 are required to induce conformational changes leading to HAV uncoating.
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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.