ArticleOncotarget2017
Viral-host interaction in kidney reveals strategies to escape host immunity and persistently shed virus to the urine.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 25 citations in OpenAlex.
- Recombinant Bacillus subtilis Displaying DHAV-1 VP1 Protein as a Dual-Function Probiotic: Evaluation of Immunological Efficacy, Growth Performance, Antioxidant Capacity, and Intestinal Health in Cherry Valley Ducks.Probiotics and antimicrobial proteins · 2026Article
- Transcriptional analysis of duck liver infected with duck hepatitis A virus type 1 isolate HA5.Frontiers in veterinary science · 2026Article
- Article
- Duck hepatitis A virus type 1 mediates cell cycle arrest in the S phase.Virology journal · 2022Article
- Catechins: Therapeutic Perspectives in COVID-19-Associated Acute Kidney Injury.Molecules (Basel, Switzerland) · 2021Review
- Mechanistic Aspects and Therapeutic Potential of Quercetin against COVID-19-Associated Acute Kidney Injury.Molecules (Basel, Switzerland) · 2020Review
- Autophagy Is a Potential Therapeutic Target Against Duck Tembusu Virus InfectionFrontiers in cellular and infection microbiology · 2020Article
- The VP3 protein of duck hepatitis A virus mediates host cell adsorption and apoptosis.Scientific reports · 2019Article
- Mutations in VP0 and 2C Proteins of Duck Hepatitis A Virus Type 3 Attenuate Viral Infection and Virulence.Vaccines · 2019Article
- Molecular detection and characterisation of feline morbillivirus in domestic cats in Malaysia.Veterinary microbiology · 2019Article
- DHAV-1 Inhibits Type I Interferon Signaling to Assist Viral Adaption by Increasing the Expression of SOCS3.Frontiers in immunology · 2019Article
- Cytokine storms are primarily responsible for the rapid death of ducklings infected with duck hepatitis A virus type 1.Scientific reports · 2018Article
- DHAV-1 2A1 Peptide - A Newly Discovered Co-expression Tool That Mediates the Ribosomal "Skipping" Function.Frontiers in microbiology · 2018Article
- Transcriptomic Characterization of a Chicken Embryo Model Infected With Duck Hepatitis A Virus Type 1.Frontiers in immunology · 2018Article
- Incompatible Translation Drives a Convergent Evolution and Viral Attenuation During the Development of Live Attenuated Vaccine.Frontiers in cellular and infection microbiology · 2018Article
- The neglected avian hepatotropic virus induces acute and chronic hepatitis in ducks: an alternative model for hepatology.Oncotarget · 2017Article
- Virologic and Immunologic Characteristics in Mature Ducks with Acute Duck Hepatitis A Virus 1 Infection.Frontiers in immunology · 2017Article
- Comparative analysis of virus-host interactions caused by a virulent and an attenuated duck hepatitis A virus genotype 1.PloS one · 2017Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis A virus is one of five types of hepatotropic viruses that cause human liver disease. A similar liver disease is also identified in ducks caused by Duck Hepatitis A virus (DHAV). Notably, many types of hepatotropic viruses can be detected in urine. However, how those viruses enter into the urine is largely unexplored. To elucidate the potential mechanism, we used the avian hepatotropic virus to investigate replication strategies and immune responses in kidney until 280 days after infection. Immunohistochemistry and qPCR were used to detect viral distribution and copies in the kidney. Double staining of CD4+ or CD8+ T cells and virus and qPCR were used to investigate T cell immune responses and expression levels of cytokines. Histopathology was detected by standard HE staining. In this study, viruses were persistently located at scattered renal tubules. No CD4+ or CD8+ T cells were recruited to the kidney, which was only accompanied by transient cytokine storms. In conclusion, the extremely scattered infection was the viral strategy to escape host immunity and may persistently shed virus into urine. The deletion of Th or Tc cell responses and transient cytokine storms indeed provide an advantageous renal environment for their persistent survival.
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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.