Loss of stress response as a consequence of viral infection: implications for disease and therapy.
Identifieur interne : 000566 ( PubMed/Corpus ); précédent : 000565; suivant : 000567Loss of stress response as a consequence of viral infection: implications for disease and therapy.
Auteurs : Philip L. Hooper ; Lawrence E. Hightower ; Paul L. HooperSource :
- Cell stress & chaperones [ 1466-1268 ] ; 2012.
English descriptors
- KwdEn :
- Animals, Diabetes Mellitus, Type 1 (metabolism), Diabetes Mellitus, Type 1 (pathology), Diabetes Mellitus, Type 1 (virology), Fatigue Syndrome, Chronic (metabolism), Fatigue Syndrome, Chronic (pathology), Fatigue Syndrome, Chronic (virology), Heat-Shock Proteins (metabolism), Hepacivirus (pathogenicity), Herpesvirus 4, Human (pathogenicity), Humans, Influenza A virus (pathogenicity), Interferons (metabolism), Neoplasms (therapy), Newcastle disease virus (pathogenicity), Simplexvirus (pathogenicity), Virus Diseases (metabolism), Virus Diseases (pathology), Virus Diseases (virology), West Nile virus (pathogenicity), eIF-2 Kinase (metabolism).
- MESH :
- chemical , metabolism : Heat-Shock Proteins, Interferons, eIF-2 Kinase.
- metabolism : Diabetes Mellitus, Type 1, Fatigue Syndrome, Chronic, Virus Diseases.
- pathogenicity : Hepacivirus, Herpesvirus 4, Human, Influenza A virus, Newcastle disease virus, Simplexvirus, West Nile virus.
- pathology : Diabetes Mellitus, Type 1, Fatigue Syndrome, Chronic, Virus Diseases.
- therapy : Neoplasms.
- virology : Diabetes Mellitus, Type 1, Fatigue Syndrome, Chronic, Virus Diseases.
- Animals, Humans.
Abstract
Herein, we propose that viral infection can induce a deficient cell stress response and thereby impairs stress tolerance and makes tissues vulnerable to damage. Having a valid paradigm to address the pathological impacts of viral infections could lead to effective new therapies for diseases that have previously been unresponsive to intervention. Host response to viral infections can also lead to autoimmune diseases like type 1 diabetes. In the case of Newcastle disease virus, the effects of viral infection on heat shock proteins may be leveraged as a therapy for cancer. Finally, the search for a specific virus being responsible for a condition like chronic fatigue syndrome may not be worthwhile if the disease is simply a nonspecific response to viral infection.
DOI: 10.1007/s12192-012-0352-4
PubMed: 22797944
Links to Exploration step
pubmed:22797944Le document en format XML
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Hooper</name><affiliation><nlm:affiliation>Division of Endocrinology, Metabolism, and Diabetes, School of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA. phoopermd@gmail.com</nlm:affiliation></affiliation></author><author><name sortKey="Hightower, Lawrence E" sort="Hightower, Lawrence E" uniqKey="Hightower L" first="Lawrence E" last="Hightower">Lawrence E. Hightower</name></author><author><name sortKey="Hooper, Paul L" sort="Hooper, Paul L" uniqKey="Hooper P" first="Paul L" last="Hooper">Paul L. 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Having a valid paradigm to address the pathological impacts of viral infections could lead to effective new therapies for diseases that have previously been unresponsive to intervention. Host response to viral infections can also lead to autoimmune diseases like type 1 diabetes. In the case of Newcastle disease virus, the effects of viral infection on heat shock proteins may be leveraged as a therapy for cancer. Finally, the search for a specific virus being responsible for a condition like chronic fatigue syndrome may not be worthwhile if the disease is simply a nonspecific response to viral infection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22797944</PMID><DateCompleted><Year>2013</Year><Month>03</Month><Day>05</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1466-1268</ISSN><JournalIssue CitedMedium="Internet"><Volume>17</Volume><Issue>6</Issue><PubDate><Year>2012</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Cell stress & chaperones</Title><ISOAbbreviation>Cell Stress Chaperones</ISOAbbreviation></Journal><ArticleTitle>Loss of stress response as a consequence of viral infection: implications for disease and therapy.</ArticleTitle><Pagination><MedlinePgn>647-55</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s12192-012-0352-4</ELocationID><Abstract><AbstractText>Herein, we propose that viral infection can induce a deficient cell stress response and thereby impairs stress tolerance and makes tissues vulnerable to damage. Having a valid paradigm to address the pathological impacts of viral infections could lead to effective new therapies for diseases that have previously been unresponsive to intervention. Host response to viral infections can also lead to autoimmune diseases like type 1 diabetes. In the case of Newcastle disease virus, the effects of viral infection on heat shock proteins may be leveraged as a therapy for cancer. 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HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:22797944" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a StressCovidV1
| This area was generated with Dilib version V0.6.33. |  |