Linked Life Data

20960373

Source:http://linkedlifedata.com/resource/pubmed/id/20960373

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-10-20
pubmed:abstractText
Hepatitis A and hepatitis C viruses (HAV and HCV) are both positive-strand ribonucleic acid (RNA) viruses with hepatotropic lifestyles. Despite several important differences, they share many biological and molecular features and similar genome replication schemes. Despite this, HAV infections are usually effectively controlled by the host with elimination of the virus, whereas HCV most often is able to establish lifelong persistent infection. The mechanisms underlying this difference are unknown. The cellular helicases RIG-I and MDA5, and Toll-like receptor 3, are pattern recognition receptors that sense virus-derived RNAs within hepatocytes in the liver. Activation of these receptors leads to their interaction with specific adaptor proteins, mitochondrial antiviral signaling protein (MAVS) and TIR-domain-containing adapter-inducing interferon-? (TRIF), respectively, which engage downstream kinases to activate two crucial transcription factors, nuclear factor kappa B (NF-?B) and interferon regulatory factor 3 (IRF3). This results in the induction of interferons (IFNs) and IFN-stimulated genes that ultimately establish an antiviral state. These signaling pathways are central to host antiviral defense and thus frequent targets for viral interference. Both HAV and HCV express proteases that target signal transduction through these pathways and that block the induction of IFNs upon sensing of viral RNA by these receptors. An understanding of the differences and similarities in the early innate immune responses to these infections is likely to provide important insights into the mechanism underlying the long-term persistence of HCV.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1098-8971
pubmed:author
pubmed:copyrightInfo
© Thieme Medical Publishers.
pubmed:issnType
Electronic
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
319-32
pubmed:meshHeading
pubmed-meshheading:20960373-Adaptive Immunity, pubmed-meshheading:20960373-Adaptor Proteins, Signal Transducing, pubmed-meshheading:20960373-Adaptor Proteins, Vesicular Transport, pubmed-meshheading:20960373-Animals, pubmed-meshheading:20960373-DEAD-box RNA Helicases, pubmed-meshheading:20960373-Hepacivirus, pubmed-meshheading:20960373-Hepatitis A, pubmed-meshheading:20960373-Hepatitis A virus, pubmed-meshheading:20960373-Hepatitis C, pubmed-meshheading:20960373-Humans, pubmed-meshheading:20960373-Immune Evasion, pubmed-meshheading:20960373-Immunity, Innate, pubmed-meshheading:20960373-Liver, pubmed-meshheading:20960373-Receptors, Pattern Recognition, pubmed-meshheading:20960373-Toll-Like Receptor 3, pubmed-meshheading:20960373-Transcription, Genetic, pubmed-meshheading:20960373-Virus Activation, pubmed-meshheading:20960373-Virus Replication
pubmed:year
2010
pubmed:articleTitle
Hepatitis A and hepatitis C viruses: divergent infection outcomes marked by similarities in induction and evasion of interferon responses.
pubmed:affiliation
Department of Medicine, The University of North Carolina, Chapel Hill, NC, USA.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural