medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: June 30, 2024
Abstract
Background
Inflammation
and
autoimmune
responses
contribute
to
the
pathophysiology
of
Long
COVID,
its
affective
chronic
fatigue
syndrome
(CFS)
symptoms,
labeled
“the
physio-affective
phenome.”
Objectives
To
investigate
whether
COVID
phenome
are
linked
autoimmunity
tight
junction
proteins,
zonulin
occludin
(ZOOC),
immune
reactivity
lipopolysaccharides
(LPS),
latter
associated
with
signs
human
herpes
virus-6
reactivation
(HHV-6),
directed
against
oligodendrocyte
neuronal
including
myelin
basic
protein
(MBP).
Methods
IgA
/
IgM/IgG
Severe
Acute
Respiratory
Syndrome
Coronavirus
2
(SARS-CoV-2),
HHV-6,
ZOOC,
C-reactive
(CRP)
advanced
oxidation
products
(AOPP),
were
measured
in
90
patients
healthy
controls.
The
was
conceptualized
as
a
factor
extracted
from
physical
symptom
domains.
Results
Neural
network
identified
LPS
(IgA-LPS),
IgG-ZOOC,
IgG-LPS,
IgA-ZOOC
most
important
variables
diagnosis
an
area
under
ROC
curve
0.755.
Partial
Least
Squares
analysis
showed
that
40.9%
variance
explained
by
CRP,
IgA-MPB
IgG-MBP.
A
large
part
variances
both
MBP
(36.3-39.7%)
(IgA
IgG)
ZOOC.
strongly
indicants
HHV-6
reactivation,
which
turn
increased
IgM-SARS-CoV-2.
Conclusions
Autoimmunity
components
junctions
bacterial
translocation
may
be
involved
COVID’s
phenome.
medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 21, 2024
Abstract
Background
Parkinson’s
disease
(PD)
is
frequently
accompanied
by
mood
and
chronic
fatigue
syndrome
(CFS)
symptoms.
It
unknown
whether
immune
activation
insulin
resistance
(IR)
or
brain
injuries
impacts
the
severity
of
affective
CFS
symptoms
due
to
PD.
Aims
To
examine
immune,
IR,
and/or
injury
biomarkers
determine
Methods
Using
a
case
(70
PD
patients)
control
(60
healthy
controls)
study
design,
we
assessed
symptoms,
measured
peripheral
immune-inflammatory
response
system
(IRS)
using
interleukin-6
(IL-6),
IL-10,
zinc,
calcium
levels,
Homeostasis
Model
Assessment
2
(HOMA2IR)
index,
serum
markers
including
S100
calcium-binding
protein
B
(S100B),
neuron-specific
enolase
(NSE),
phosphorylated
tau217
(pTau217),
glial
fibrillary
acidic
(GFAP).
Results
patients
showed
increased
scores,
IRS
activation,
HOMA2IR,
NSE,
GFAP,
pTau217,
S100B
levels
as
compared
controls.
A
large
part
(52.5%)
variance
in
mood+CFS
score
was
explained
regression
on
S100B,
HOMA2IR
interleukin-10
(IL-10)
(all
positively)
(inversely).
The
indices
were
significantly
associated
with
all
4
biomarkers.
latter
(37.0%)
cumulative
effects
indices.
Discussion
RS
IR
contribute
damage
cell
projections
type
III
intermediate
filament,
which
turn
medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: June 30, 2024
Abstract
Background
Inflammation
and
autoimmune
responses
contribute
to
the
pathophysiology
of
Long
COVID,
its
affective
chronic
fatigue
syndrome
(CFS)
symptoms,
labeled
“the
physio-affective
phenome.”
Objectives
To
investigate
whether
COVID
phenome
are
linked
autoimmunity
tight
junction
proteins,
zonulin
occludin
(ZOOC),
immune
reactivity
lipopolysaccharides
(LPS),
latter
associated
with
signs
human
herpes
virus-6
reactivation
(HHV-6),
directed
against
oligodendrocyte
neuronal
including
myelin
basic
protein
(MBP).
Methods
IgA
/
IgM/IgG
Severe
Acute
Respiratory
Syndrome
Coronavirus
2
(SARS-CoV-2),
HHV-6,
ZOOC,
C-reactive
(CRP)
advanced
oxidation
products
(AOPP),
were
measured
in
90
patients
healthy
controls.
The
was
conceptualized
as
a
factor
extracted
from
physical
symptom
domains.
Results
Neural
network
identified
LPS
(IgA-LPS),
IgG-ZOOC,
IgG-LPS,
IgA-ZOOC
most
important
variables
diagnosis
an
area
under
ROC
curve
0.755.
Partial
Least
Squares
analysis
showed
that
40.9%
variance
explained
by
CRP,
IgA-MPB
IgG-MBP.
A
large
part
variances
both
MBP
(36.3-39.7%)
(IgA
IgG)
ZOOC.
strongly
indicants
HHV-6
reactivation,
which
turn
increased
IgM-SARS-CoV-2.
Conclusions
Autoimmunity
components
junctions
bacterial
translocation
may
be
involved
COVID’s
phenome.
