Loss of stress response as a consequence of viral infection: implications for disease and therapy.
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.
Division of Endocrinology, Metabolism, and Diabetes, School of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA. phoopermd@gmail.com
Philip L
PL
Hooper
Lawrence E
LE
Hightower
Paul L
PL
Hooper
D000818:Animals; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism / Q000473:pathology / Q000821:virology; D015673:Fatigue Syndrome, Chronic / Q000378:metabolism / Q000473:pathology / Q000821:virology; D006360:Heat-Shock Proteins / Q000378:metabolism*; D016174:Hepacivirus / Q000472:pathogenicity; D004854:Herpesvirus 4, Human / Q000472:pathogenicity; D006801:Humans; D009980:Influenza A virus / Q000472:pathogenicity; D007372:Interferons / Q000378:metabolism; D009369:Neoplasms / Q000628:therapy; D009522:Newcastle disease virus / Q000472:pathogenicity; D018139:Simplexvirus / Q000472:pathogenicity; D014777:Virus Diseases / Q000378:metabolism / Q000473:pathology / Q000821:virology*; D014902:West Nile virus / Q000472:pathogenicity; D019892:eIF-2 Kinase / Q000378:metabolism
D006360:Heat-Shock Proteins; D007372:Interferons; D019892:eIF-2 Kinase