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Is een verminderde

fysiologische stressresponse

het gevolg van

virale infecties?






Onlangs verscheen een interessant artikel van de hand van Philip Hooper en collega's

waarin een slechte (fysiologische) stressresponse gerelateerd wordt aan virale infecties.


Volgens de auteurs leiden virale infecties soms tot een afname van heat shock proteÔnen.

Daardoor zijn patiŽnten mogelijk fysiologisch minder goed in staat op stress te reageren.


Los van de interessante vraag of virale infecties de oorzaak zijn, is eerder door anderen vastgesteld dat de heat shock proteÔnen-respons op inspanning in ME/CVS aanzienlijk

minder is (klik hier en hier) en dat dit vooral bij postvirale ME/CVS een rol speelt (klik hier).




Citaten uit de studie:



Unlike eukaryotes and bacteria, viruses do not have heat shock proteins (Hsps) and rely on host Hsps for viral protein folding. As a result, processes that regulate host stress proteins are likely targets of strategic manipulation by both viruses and infected hosts.




Activated PKR arrests protein synthesis and Hsp translation via phosphorylation of translation initiation factor eIF2a.




In particular, infectious impair≠ment of the stress response, as the examples we have described herein suggest, could make subjects vulnerable to even minor stresses and injury.




If CFS symptoms reflect an impaired Hsp state, then improving the Hsp re≠sponse should improve the condition. Indeed, a nutraceutical product (ADAPT-232 forte), which combines extracts from three herbs (Eleutherococcus senticosus, Schizandra chinensis, and Rhodiola rosea), raises Hsps in response to exercise.




It is worth noting, however, that while raising Hsps may be protective in the case of some viral infections, in other cases, increasing Hsps could, theoretically, augment viral replication.






Loss of stress response as a consequence of viral infection:

implications for disease and therapy.

Cell Stress Chaperones. 2012 Jul 14. doi: 10.1007/s12192-012-0352-4.

Hooper PL, Hightower LE, Hooper PL.





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.



PMID: 22797944