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 proteïnen.
Daardoor zijn patiënten 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 proteïnen-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 impairment 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 response 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.
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.
PMID: 22797944
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