ArticleThe Journal of clinical investigation2011
A polymorphism in TIM1 is associated with susceptibility to severe hepatitis A virus infection in humans.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 86 citations in OpenAlex.
- Autoantibodies neutralizing type I IFNs in patients with fulminant herpes simplex virus hepatitis.The Journal of experimental medicine · 2026Article
- Genetic and autoimmune predispositions to fulminant viral hepatitis in children.Frontiers in immunology · 2026Review
- Review
- Up-regulation of blood-circulating TIM-4-expressing monocytes and potential diagnostic biomarker sTIM-4 in primary liver cancer.Scientific reports · 2025Article
- Redefining the immune landscape of hepatitis A virus infection.Experimental & molecular medicine · 2025Review
- An Integrated Analysis of HAVCR1 with a Focus on Immunological and Prognostic Roles in Breast Cancer.Cancer informatics · 2025Article
- Molecular Basis for the Differential Function of HAVCR1 Mucin Variants.Biomedicines · 2024Article
- Hepatitis A virus infection.Nature reviews. Disease primers · 2023Review
- Review
- A pan-cancer analysis of HAVCR1 with a focus on diagnostic, prognostic and immunological roles in human cancers.American journal of translational research · 2023Article
- Single Nucleotide Variants of the Human TIM-1 IgV Domain with Reduced Ability to Promote Viral Entry into Cells.Viruses · 2022Article
- TIM-1 Augments Cellular Entry of Ebola Virus Species and Mutants, Which Is Blocked by Recombinant TIM-1 Protein.Microbiology spectrum · 2022Article
- Mechanisms of Hepatocellular Injury in Hepatitis A.Viruses · 2021Review
- Kidney Injury Molecule 1 (KIM-1): a Multifunctional Glycoprotein and Biological Marker (Review).Sovremennye tekhnologii v meditsine · 2021Review
- Hepatitis A virus survival on drug paraphernalia.Journal of viral hepatitis · 2020Article
- Tim-4 functions as a scavenger receptor for phagocytosis of exogenous particles.Cell death & disease · 2020Article
- Human genetic basis of fulminant viral hepatitis.Human genetics · 2020Review
- [Advances in the pathogenesis of pre-hepatic failure].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020Article
- Genetic polymorphisms of rs9313422 G>C and rs41297579 G>A at the promoter of TIM-1 gene contribute to the risk of community-acquired pneumonia in children.Journal of clinical laboratory analysis · 2020Article
- Adaptive Immune Responses in Hepatitis A Virus and Hepatitis E Virus Infections.Cold Spring Harbor perspectives in medicine · 2019Review
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15 authors at 6 institutions in 2 countries.
Funding
Abstract
During infection with the hepatitis A virus (HAV), most patients develop mild or asymptomatic disease. However, a small number of patients develop serious, life-threatening hepatitis. We investigated this variability in disease severity by examining 30 Argentinean patients with HAV-induced acute liver failure in a case-control, cross-sectional, observational study. We found that HAV-induced severe liver disease was associated with a 6-amino-acid insertion in TIM1/HAVCR1 (157insMTTTVP), the gene encoding the HAV receptor. This polymorphism was previously shown to be associated with protection against asthma and allergic diseases and with HIV progression. In binding assays, the TIM-1 protein containing the 157insMTTTVP insertion polymorphism bound HAV more efficiently. When expressed by human natural killer T (NKT) cells, this long form resulted in greater NKT cell cytolytic activity against HAV-infected liver cells, compared with the shorter TIM-1 protein without the polymorphism. To our knowledge, the 157insMTTTVP polymorphism in TIM1 is the first genetic susceptibility factor shown to predispose to HAV-induced acute liver failure. Furthermore, these results suggest that HAV infection has driven the natural selection of shorter forms of the TIM-1 protein, which binds HAV less efficiently, thereby protecting against severe HAV-induced disease, but which may predispose toward inflammation associated with asthma and allergy.
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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.