e
p
o
s
a
ú
d
e
p
ú
b
l
i
c
a
.
2
0
1
4;3
2(1):18–26
www.else ie .p / psp
O iginal
A icle
Associa ion
be ween
ch onic
s ess
and
immune
esponse
o
influenza
accine
in
heal hca e
wo ke s
Ema
Sacadu a-Lei ea,b,c,∗,
An ónio
Sousa-U ab,c,
Helena
Rebelo-de-And aded,e,
Sancha
Fe ei aa,
Regina
Rochaa
aOccupa ional
Heal h
Depa men
o
Hospi al
de
San a
Ma ia/CHLN,
Lisbon,
Po ugal
bNa ional
School
o
Public
Heal h/New
Uni e si y
o
Lisbon,
Lisbon,
Po ugal
cCMDT
–
Cen o
de
In es igac¸ão
da
Malá ia
e
Doenc¸as
T opicais
–
Public
Heal h,
Lisbon,
Po ugal
dNa ional
Ins i u e
o
Heal h,
INSA,
Lisbon,
Po ugal
eFacul y
o
Pha macy,
Uni e si y
o
Lisbon,
Lisbon,
Po ugal
a
i
c
l
e
i
n
o
A icle
his o y:
Recei ed
15
Ap il
2013
Accep ed
27
Sep embe
2013
A ailable
online
19
Decembe
2013
Keywo ds:
An ibody
esponse
Heal hca e
wo ke s
Influenza
accine
Psychological
s ess
a
b
s
a
c
In oduc ion:
Ch onic
s ess
can
influence
immune
esponse
o
accines.
Heal hca e
wo ke s
a e
exposed
o
s esso s
and
biological
haza ds,
he
heal h
e ec s
o
which
may
be
p e en ed
h ough
accina ion.
Objec i es:
This
s udy
aims
o
e alua e
he
associa ion
be ween
s ess
in
nu ses
and:
(1)
insu ficien
esponse
o
influenza
accine,
assessed
one
mon h
a e
accina ion
(T1);
(2)
he
d op
in
haemagglu ina ion-inhibi ion
(HAI)
an ibodies
(ab)
six
mon hs
a e
accina ion
(T6).
Me hods:
A
nes ed
case–con ol
s udy
was
ca ied
ou
wi h
136
heal hy
hospi al
nu ses.
Indi idual
in e iews,
he
Gene al
Heal h
Ques ionnai e
(GHQ12)
and
Maslach
Bu nou
In en o y
(MBI-HSS)
we e
applied
in
o de
o
de e mine
he
p esence
o
s ess,
using
he
iangula ion
me hod
a
he
beginning
o
he
s udy
(T0).
Influenza
accine
was
adminis e ed
and
i es
o
HAI
abo e
each
s ain
composing
influenza
accine
be o e
accina ion
(T0),
a
T1and
T6
we e
assessed.
Resul s:
The e
was
no
s a is ically
ele an
(5%)
ela ionship
be ween
s ess
and
he
insu fi-
cien
immune
esponse
o
he
accine
a
T1.
Ne e heless,
he e
was
an
associa ion
be ween
s ess
and
he
d op
in
HAI
ab
AH1a
T6,
when
we
assessed
s ess
by
he
iangula ion
me hod
using
an
in e iew
(p
=
0.006),
GHQ12 (p
=
0.045)
and
combina ion
o
c i e ia
(p
=
0.001),
e en
a e
mul i a ia e
analysis
( espec i ely,
p
=
0.01,
p
<
0.05
and
p
=
0.002).
The
odds
a ios
we e,
espec i ely,
3.64,
2.73
and
5.22.
Conclusions:
The
associa ion
we
ound,
be ween
ch onic
s ess
and
he
d op
in
HAI
ab
a
T6,
co obo a es
he
hypo hesis
ha
s ess
can
nega i ely
influence
immune
esponse.
The e o e,
i
seems
easonable
o
conside
his
issue
when
we
implemen
accina ion
p og ammes
o
heal hca e
wo ke s.
©
2013
Escola
Nacional
de
Saúde
Pública.
Published
by
Else ie
España,
S.L.
All
igh s
ese ed.
∗Co esponding
au ho .
E-mail
add ess:
[email p o ec ed].p
(E.
Sacadu a-Lei e).
0870-9025/$
–
see
on
ma e
©
2013
Escola
Nacional
de
Saúde
Pública.
Published
by
Else ie
España,
S.L.
All
igh s
ese ed.
h p://dx.doi.o g/10.1016/j. psp.2013.09.002
e
p
o
s
a
ú
d
e
p
ú
b
l
i
c
a
.
2
0
1
4;3
2(1):18–26
19
S esse
c ónico
e
a
imunidade
à
acina
con a
a
g ipe
em
p ofissionais
de
saúde
Pala as-cha e:
An ico pos
P ofissionais
de
saúde
Vacina
con a
a
g ipe
S esse
e
s
u
m
o
In oduc¸ão:
O
s esse
c ónico
pode
influencia
a
espos a
imuni á ia
à
acinac¸ão.
Os
p ofis-
sionais
de
saúde
es ão
expos os
a
s esso es
de
na u eza
p ofissional
e
ainda
a
agen es
biológicos
cujos
e ei os
pode ão
se
p e enidos
pela
acinac¸ão.
Obje i os:
Es uda
a
associac¸ão
en e
a
p esenc¸a
de
s esse
e
(1)
a
“insuficien e”
espos a
imuni á ia
à
acina
con a
a
g ipe,
a aliada
um
mês
após
a
acinac¸ão
(T1);
(2)
a
educ¸ão
dos
í ulos
de
an ico pos
di igidos
às
hemaglu ininas
(HAI)
seis
meses
após
a
acinac¸ão
(T6).
Mé odos:
Realizou-se
um
es udo
caso-con olo
inco po ado
num
es udo
de
coo es
com
a
pa icipac¸ão
de
136
en e mei os
hospi ala es
saudá eis.
Realiza am-se
en e is as
indi idu-
ais
e
aplica am-se
os
ques ioná ios
The
Gene al
Heal h
Ques ionnai e
(GHQ12)
e
Maslach
Bu nou
In en o y
(MBI-HSS)
pa a
de e minac¸ão
da
p esenc¸a
de
s esse
c ónico
pelo
mé odo
da
iangulac¸ão,
no
início
do
es udo
(T0).
Foi
adminis ada
a
acina
con a
a
g ipe
e
de e minou-
se
os
í ulos
de
HAI
di igidos
a
cada
es i pe
componen es
da
acina
con a
a
g ipe,
an es
da
acinac¸ão(T0),
em
T1e
em
T6.
Resul ados:
Não
se
encon ou
associac¸ão
significa i a
(5%)
en e
a
p esenc¸a
de
s ess
e
a
“insuficien e”
espos a
à
acina
con a
a
g ipe
em
T1.
Con udo,
encon ou-se
uma
associac¸ão
en e
a
p esenc¸a
de
s ess
e
a
diminuic¸ão
do
í ulo
de
HAI
di igidos
à
es i pe
A(H1N1)
em
T6
quando
se
a aliou
a
p esenc¸a
de
s esse
pelo
mé odo
da
iangulac¸ão
usando
a
en e is a
(p=0,006),
o
GHQ12 (p=0,045)
e
a
combinac¸ão
dos
ês
c i é ios
(p=0,001),
que
se
man e e
após
análise
mul i a iada
( espe i amen e
p=0,01,
p<0.05
e
p=0.002).
Os
odds
a io
ajus ados
o am
de
3,64,
de
2,73
e
de
5,22.
Conclusões:
A
associac¸ão
encon ada
en e
a
p esenc¸a
de
s esse
c ónico
e
a
educ¸ão
do
í ulo
de
HAI
em
T6 em
apoia
a
hipó ese
de
que
o
s esse
pode á
influencia
nega i a-
men e
a
manu enc¸ão
dos
í ulos
de
an ico pos,
mesmo
em
indi íduos
adul os
não
idosos.
Assim,
pa ece
azoá el
conside a
es e
aspe o
quando
se
p e ende
implemen a
p og amas
de
acinac¸ão
di igidos
a
p ofissionais
de
saúde.
©
2013
Escola
Nacional
de
Saúde
Pública.
Publicado
po
Else ie
España,
S.L.
Todos
os
di ei os
ese ados.
In oduc ion
Heal hca e
wo ke s
a e
exposed
o
many
s esso s,
some
o
hem
ela ed
wi h
o ganisa ional
wo k
condi ions
and
o he s,
mo e
specific
o
his
p o ession,
ela ed
wi h
hei
ac i i y
o
ca ing
o
he
ill.1–3
Ch onic
s ess
and
bu nou
seem
o
be
e y
common
in
nu ses.4–6 Fo
example,
López-Cas illo
and
colleagues
ound
high
le els
o
emo ional
dis u bance
de e mined
by
he
Gen-
e al
Heal h
Ques ionnai e
(GHQ28)
in
39%
o
hospi al
nu ses.7
Amongs
he
consequences
o
ch onic
dis ess,
whe he
hey
a e
ela ed
o
no
wi h
wo k,
a e
he
possible
e ec s
on
he
immune
sys em,
including
e ec s
on
he
immune
esponse
o
accina ion.
Heal hca e
wo ke s
a e
s ongly
ad ised
o
be
accina ed
agains
influenza
in
o de
o
p o ec
hemsel es
agains
he
disease,
educe
s a
absen eeism
and
minimise
he
isk
o
nosocomial
ansmission
o
he
pa ien s
hey
ake
ca e
o .
Vaccina ion
is
a
possible
model
o
immune
esponse,
es -
ing
mos ly
he
humo al
immune
esponse.
Vaccina ed
people
de elop
an ibodies
(ab)
ha
bind
and
neu alise
he
i us,
in
mos
cases
ab
agains
he
su ace
glycop o ein
hemagglu-
inin.
Those
ab
can
be
used
as
ma ke s
o
p o ec ion
agains
he
disease,8caused
by
s ains
ha
a e
simila
o
he
accine
composi ion.
Acco ding
o
me a-analysis
by
Sege s om
and
Mille ,
ch onic
exposu e
o
s esso s
such
as
aking
ca e
o
spouses
wi h
demen ia,
unemploymen
and
su e ing
om
physi-
cal
disabili y
is
associa ed
wi h
a
smalle
ab
esponse
o
influenza
accine.9Some
e iews
also
sugges
ha
ch onic
s ess
is
associa ed
wi h
a
smalle
ab
esponse
o
influenza
accine.10–12
Gene ally
speaking,
s udies
e alua ing
he
associa ion
be ween
ch onic
s ess
and
immune
esponse
o
influenza
accine
showed
ela i ely
consis en
esul s
in
old
people.
In
hose
people,
ch onic
exposu e
o
s esso s
was
associ-
a ed
wi h
ch onic
anxie y
and
symp oms
o
dep ession
and
a
lowe
esponse
o
influenza
accine,
in
compa ison
o
a
con-
ol
g oup.13–17
The
use
o
a
s anda dized
dose
o
an igen
which
p omo es
a
good
immune
esponse
in
mos
adul s,
could
make
i
di -
ficul
he
de ec ion
o
he
influence
o
ch onic
s ess
in
he
immune
esponse
o
accina ion
in
younge
adul s,
wi h
a
obus
immune
sys em.
Olde
people
ha e
a
weake
immune
sys em,
ela ed
wi h
age,
so
his
could
be
an
explana ion
o
he
g ea e
con-
sis ency
o
esul s
showing
a
nega i e
associa ion
be ween
ch onic
s ess
and
immune
esponse
o
accines
in
hem.
Vedha a
and
colleagues
did
no
find
any
associa ion
be ween
aking
ca e
o
spouses
wi h
mul iple
scle osis
and
ab
esponse
o
influenza
accine
in
adul s
unde
he
age
o
55.18
20
e
p
o
s
a
ú
d
e
p
ú
b
l
i
c
a
.
2
0
1
4;3
2(1):18–26
Howe e ,
hose
adul s
showed
simila
s ess
le els
as
he
con-
ol
g oup.
In
younge
adul s,
such
as
uni e si y
s uden s,
some
s udies19–22 ound
an
associa ion
be ween
s ess,
cha ac-
e ised
in
di e en
ways,
and
he
immune
esponse
o
influenza
accine
(assessed
by
ab
i es
o
by
esponse
a e)
one
mon h
a e
accina ion.
Howe e ,
o he
s udies
did
no
find
ha
associa ion.23–25
Some
o
he
s udies
ound
an
associa ion
be ween
s ess
and
a
d op
in
ab
i es
assessed
4–6
mon hs
a e
accina ion,19–23,25 e en
in
he
younges
adul s.
The
d op
in
he
ab
i es
associa ed
wi h
s ess
was
only
obse ed
agains
one
s ain
o
accine
componen s,
sugges ing
ha
di e en
exposu es
o
di e en
pas
accina ions
can
be
esponsible
o
hose
esul s.
In
an
occupa ional
con ex
o
heal hca e
se ings,
whe e
heal hca e
wo ke s
a e
in
he
labou
ma ke
(and
a e
he e-
o e
no
e y
old),
bu
a e
simul aneously
exposed
o
ch onic
s esso s
and
biological
isk
haza ds,
i
seems
impo an
o
s udy
he
influence
o
s ess
on
immune
esponse
o
influenza
accine.
The e o e,
his
s udy
analyses
he
associa ion
be ween
s ess
in
nu ses
and:
(1)
insu ficien
esponse
o
influenza
ac-
cine,
assessed
one
mon h
a e
accina ion
(T1);
(2)
he
d op
in
influenza
aemagglu ina ion-inhibi ion
(HAI)
ab
i es
six
mon hs
a e
accina ion
(T6),
as
compa ed
o
one
mon h
pos
accina ion
HAI
ab
i es.
Ma e ials
and
me hods
S udy
design
and
pa icipan s
The
s udy
was
a
nes ed
case–con ol
s udy,
conduc ed
o e
six
mon hs
in
a
uni e si y
hospi al
du ing
he
2007/2008
influenza
season.
Subjec s
we e
hospi al
nu ses
who
we e
no
aking
any
egula
medica ion,
including
d ugs
ha
could
a ec
immu-
ni y
(such
as
cance
he apy
d ugs
o
co icos e oids).
They
did
no
ha e
any
medical
condi ion
ha
could
a ec
he
immune
esponse
and
hey
also
had
no
majo
su ge y
in
he
p eceding
h ee
mon hs.
They
did
no
ha e
a
his o y
o
d ug
consump-
ion
o
alcohol
consump ion
g ea e
han
10
uni s
pe
week,
no
did
hey
handle
ci o oxic
d ugs
o
wo k
egula ly
wi h
ionising
adia ion
(n
=
136).
The
hospi al’s
E hics
Commi ee
app o ed
he
s udy
and
all
he
pa icipan s
signed
hei
ag ee-
men
o
pa icipa ing
in
i .
One-mon h
and
six-mon h
d op-ou
c i e ia:
•
clinical
diagnosis
o
medical
condi ion
ha
may
a ec
immune
esponse
a e
he
beginning
o
he
s udy
o
aking
any
egula
medica ion
ha
can
a ec
immuni y
(assessed
by
in e iew,
a
T1and
T6);
•
wo kplace
changes
wi h
egula
exposu e
o
ionising
adia-
ions
o
ci o oxic
d ugs
handling;
•
clinical
influenza
symp oms
wi h
i us
iden ifica ion
in
nasal
o
o opha yngeal
swab,
du ing
he
six
mon hs
o
he
s udy;
•
a
ise
in
HAI
Ab
i e
o
A(H1N1),
A(H3N2)
o
B
s ains
six
mon hs
a e
accina ion,
as
compa ed
wi h
he
i es
mea-
su ed
one
mon h
a e
accina ion.
Such
a
ise
in
HAI
Ab
i e
sugges s
an
exposu e
o
influenza
s ains
du ing
T1and
T6ins ead
o
a
delayed
esponse
o
he
accine.
S ess
assessmen
S uc u ed
indi idual
in e iews
we e
conduc ed
a
he
begin-
ning
o
he
s udy
(T0)
in
o de
o:
•
iden i y
socio-demog aphic
cha ac e is ics
and
possible
con oundable
a iables
ela ed
wi h
immuni y
(physical
exe cise,
nu i ional
pa ame e s,
nu i ional
supplemen s,
hou s
o
sleep
pe
day,
smoking
habi s,
shi
wo k)
and
influenza
accina ion
his o y;
•
iden i y
wo k- ela ed
and
non-wo k- ela ed
s esso s,
using
a
Like
scale
om
1
o
5;
•
assess
pe cei ed
s ess,
using
a
Like
scale
om
1
o
5;
•
iden i y
s ess- ela ed
beha iou al
changes
o
psychoso-
ma ic
symp oms.
We
also
applied
he
Po uguese
e sions
o
he
Gene al
Heal h
Ques ionnai e
(GHQ12)
and
Maslach
Bu nou
In en o y
(MBI-HSS
o
MBI)
exhaus ion
scale
a
he
beginning
o
he
s udy
(T0).
Al a
C onbach
o
hose
scales
was
0.855
and
0.874
espec i ely.
In
o de
o
assess
he
p esence
o
ch onic
s ess,
we
applied
he
iangula ion
me hod
a
T0,
as
sugges ed
by
Cox
and
colleagues,26 in
ou
di e en
ways:
•
h ough
in e iews:
we
accep ed
he
p esence
o
ch onic
s ess
using
in e iews
i
he e
we e
iden ified
s esso s
classified
as
4
o
5,
plus
pe cei ed
s ess
classified
as
4
o
5,
plus
a
leas
one
beha iou al
change
o
one
psychosoma ic
symp om
s ess- ela ed;
•
h ough
GHQ12:
we
accep ed
he
p esence
o
ch onic
s ess
using
GHQ12 i
he e
we e
iden ified
s esso s
classified
as
4
o
5,
plus
GHQ12 highe
han
2,
plus
a
leas
one
beha iou al
change
o
one
psychosoma ic
symp om
s ess- ela ed;
•
h ough
MBI:
we
accep ed
he
p esence
o
ch onic
s ess
using
MBI
i
he e
we e
iden ified
s esso s
classified
as
4
o
5,
plus
MBI
exhaus ion
scale
highe
han
24,
plus
a
leas
one
beha iou al
change
o
one
psychosoma ic
symp om
s ess-
ela ed;
•
combina ion
o
c i e ia:
we
accep ed
he
p esence
o
s ess
using
combina ion
o
c i e ia
i
he e
was
s ess
using
in e -
iew
and
s ess
using
GHQ12 o
i
he e
was
s ess
using
in e iew
and
s ess
using
MBI
exhaus ion
scale.
Vaccina ion
and
labo a o y
p ocedu es
Venous
blood
was
d awn
a
h ee
s ages
be ween
Oc obe
2007
and
Ap il
2008:
(i)
immedia ely
be o e
influenza
acci-
na ion
(T0);
(ii)
one
mon h
ollowing
immunisa ion
(T1);
and
(iii)
six
mon hs
a e
T0(T6).
The
samples
es ed
1
h
a
ambien
empe a u e
ollow-
ing
cen i uga ion
a
3500
pm
o
10
min.
Se a
we e
s o ed
a
−20 ◦C
un il
used.
All
he
samples
d awn
a
T0,
T1and
T6we e
p ocessed
a
he
same
ime
and
unde
he
same
condi ions.
A
comme cially
a ailable
2007/2008
i alen
influenza
ac-
cine,
wi h
he
ecommended
composi ion
o
ha
season
in
No h
Hemisphe e,
was
adminis e ed
in amuscula ly,
in
he
e
p
o
s
a
ú
d
e
p
ú
b
l
i
c
a
.
2
0
1
4;3
2(1):18–26
21
del oid
muscle,
du ing
Oc obe .
All
he
accines
belonged
o
he
same
g oup
(AFLUA290AD).
Haemagglu ina ion
inhibi ion
eac ion
was
used
o
assess
specific
HAI
ab
i e
agains
influenza
A(H1N1),
A(H3N2)
and
B
s ains
included
in
he
influenza
accine,
in
acco dance
wi h
he
Wo ld
Heal h
O ganisa ion’s
manual.27 Immedia ely
be o e
he
labo a o ial
p ocedu es,
he
se a
we e
ea ed
by
a
Recep o -Des oying
Enzyme
(RDE)
in
o de
o
emo e
unspecific
agglu inins
and
inhibi o s.
The
e e ence
an igens
we e
dilu ed
o
ob ain
4
uni s
agains
haemmaglu inin
pe
25
␮l
and
incuba ed
wi h
he
ea ed
se a
samples.
E y h ocy es
we e
hen
added
o
he
fluid.
HAI
Ab
i e
co esponded
o
he
in e se
o
he
las
dilu ion
o
se um
ha
comple ely
inhibi ed
haemagglu ina ion.
We
used
p og essi e
dilu ions,
s a ing
wi h
1:10
up
o
1:20.480.
The
se ological
pa ame e s
ob ained
we e:
•
HAI
Ab
i e
agains
influenza
A(H1N1),
A(H3N2)
and
B
s ains
included
in
influenza
accine,
be o e
(T0)
and
a e
accina ion
(T1and
T6);
•
ise
in
HAI
Ab
i e
agains
influenza
A(H1N1),
A(H3N2)
and
B
s ains
included
in
influenza
accine,
assessed
one
mon h
a e
accina ion
(compa ed
o
HAI
Ab
i e
immedia ely
be o e
accina ion);
•
d op
in
HAI
Ab
i e
agains
influenza
A(H1N1),
A(H3N2)
and
B
s ains
included
in
influenza
accine,
be ween
T1and
T6.
Defini ions
Fo
analysis
a
T1and
a
T6,
we
defined
he
ollowing
g oups:
esponde s
a
T1(one
mon h
a e
accina ion):
pa icipan s
ha
showed,
a
T1,
a
leas
a
ou old
ise
in
HAI
ab
i e
compa ed
o
he
i e
be o e
accina ion;
non- esponde s
a
T1(one
mon h
a e
accina ion):
pa ic-
ipan s
ha
did
no
show,
a
T1,
a
ou old
ise
in
HAI
ab
i e
compa ed
o
he
i e
be o e
accina ion;
HAI
ab
i e
d op
g oup
a
T6(six
mon hs
a e
accina ion):
pa icipan s
wi h
a
leas
a
ou old
ise
in
HAI
ab
i e
a
T1,
bu
who
showed
a
d op
in
HAI
ab
i e
a
T6,
as
compa ed
o
HAI
ab
i e
a
T1;
no
change
in
HAI
ab
i e
g oup
a
T6(six
mon hs
a e
ac-
cina ion):
pa icipan s
wi h
a
leas
a
ou old
ise
in
HAI
ab
i e
a
T1,
bu
wi h
no
change
in
HAI
ab
i e
a
T6,
as
compa ed
o
HAI
ab
i e
a
T1.
S a is ical
analyses
Fo
dicho omous
a iables,
we
used
he
Qui-squa e
and
Fishe
exac
es s
and
de e mined
he
odds
a io.
Fo
nume ical
a iables,
we
used
he
Kolmogo o –Smi no
and
Shapi o–Wilk
es s
o
assess
no mal
dis ibu ion
in
non-
esponde s
and
esponde s
(T1)
and
in
he
HAI
Ab
i e
d op
g oup
and
no
change
in
HAI
Ab
i e
g oup
(T6).
Fo
no mal
dis ibu ions,
he
T
S uden
es
was
used
o
compa e
means,
and
he
Le ene
es
o
assess
a iance
homogenei y.
Fo
no
no mal
dis ibu ions,
we
applied
he
Mann–Whi ney
es
o
compa e
medians.
We
also
used
he
mul i a ia e
analysis
and
de e mined
he
adjus ed
odds
a io
o
he
con ounding
a iables.
We
conside ed
a
s a is ical
significance
o
5%.
All
es s
we e
un
in
he
S a is ical
Package
o
Social
Sciences
–
SPSS®so wa e,
e sion
14.0
o
Windows.
Resul s
We
s udied
136
nu ses,
mos
o
whom
we e
emale
(83.8%),
Caucasian
(96.3%)
and
did
no
smoke
(77.9%).
Thei
a e age
age
was
33
and
he
median
age
was
29
(22–63
yea s
old).
Only
one
pa icipan
was
mo e
han
six y
yea s
o
age.
Mo e
han
one
hal
o
he
pa icipan s
had
been
gi en
an
influenza
accine
sho
a
leas
one
o
he
ou
seasons
p io
o
he
beginning
o
he
s udy
(52.9%),
mos ly
in
he
yea
imme-
dia ely
be o e
(44.1%).
Nu ses
included
in
he
s udy
wo ked
mos ly
on
a
shi
wo k
basis
(70.6%),
had
a
co po al
index
mass
(kg/m2)
be ween
18.5
and
24.9
(72.1%)
and
slep
a
leas
7
h
pe
day
(66.2%).
The
majo i y
did
no
ake
i amin
supplemen s
(86.8%)
o
fish
oil
(98.5%).
Only
54.4%
did
egula
physical
exe -
cise
and
46.3%
a e
yogu
daily.
Associa ion
be ween
ch onic
s ess
and
non- esponde s
a
T1
One
mon h
a e
accina ion
(T1),
we
did
no
find
any
associ-
a ion
o
s a is ical
significance
be ween
non- esponde s
o
A(H1N1)
i us
s ain
included
in
he
influenza
accine
and
he
p esence
o
ch onic
s ess
a
T0,
assessed
in
ou
di e -
en
ways.
Simila ly,
he e
was
also
no
associa ion
be ween
non- esponde s
o
A(H3N2)
o
non- esponde s
o
B
s ains
included
in
he
influenza
accine
and
ch onic
s ess
a
T0.
To
simpli y
he
able,
we
named
esponde s
o
non- esponde s
o
A(H1N1)
and
o
A(H3N2)
as
esponde s
o
non- esponde s
AH1and
AH3 espec i ely
(Table
1).
Aemagglu ina ion-inhibi ion
an ibodies
i es
a
T0in
esponde s
and
non- esponde s
a
T1
Using
he
Kolmogo o –Smi no
and
Shapi o–Wilk
es s,
we
ound
ha
he e
is
no
no mal
dis ibu ion
in
non- esponde s
and
esponde s
a
T1 o
he
conside ed
con inuous
a iables
(p
<
0.001).
The e o e,
we
applied
he
Mann–Whi ney
es
o
compa e
medians
be ween
HAI
ab
i es
a
T0in
esponde s
and
non- esponde s
a
T1.
We
ound
ha
non- esponde s
AH1a
T1had
significan ly
highe
HAI
ab
AH1 i es
a
T0
han
esponde s
AH1a
T1.
The
same
happened
wi h
non-
esponde s
AH3a
T1and
non- esponde s
B
a
T1,
who
had
significan ly
highe
HAI
AH3 i es
a
T0and
HAI
B
i es
a
T0
han
he
co esponding
esponde s
(Table
2).
Associa ion
be ween
ch onic
s ess
and
d op
in
aemagglu ina ion-inhibi ion
ab
i es
a
T6
A
T6(six
mon hs
a e
accina ion),
he
p esence
o
s ess
in
he
HAI
ab
AH1 i e
d op
g oup
was
highe
han
in
he
no
change
in
HAI
ab
AH1 i e
g oup,
when
we
assessed
s ess
by
all
he
conside ed
di e en
ways,
being
s a is ically
signi-
fica i e
when
we
assessed
he
p esence
o
ch onic
s ess
by
22
e
p
o
s
a
ú
d
e
p
ú
b
l
i
c
a
.
2
0
1
4;3
2(1):18–26
Table
1
–
S ess
in
non- esponde s
and
in
esponde s
AH1,
AH3and
B
a
T1.
HAI
ab
g oups
a
T1Ch onic
s ess
assessmen
S ess
in
non- esponde s
a
T1
S ess
in
esponde s
a
T1
S a is ical
analysis
(Qui-squa e
es )
n
(%)
n
(%)
OR
(95%
CI)
p
AH1(n
=
135)
Non- esponde s:
45
Responde s:
90
S ess
(in e iew)
28
(62.2)
46
(51.1)
1.575
(0.759–3.272)
0.221
S ess
(GHQ12)a19
(42.2)
44
(48.9)
0.764
(0.371–1.572)
0.464
S ess
(MBI)b16
(35.6)
36
(40.0)
0.828
(0.394–1.738)
0.617
S ess
(combina ion
o
c i e ia)c20
(44.4)
41
(45.6)
0.956
(0.466–1.963)
0.903
AH3(n
=
136)
Non- esponde s:
50
Responde s:
86
S ess
(in e iew)
27
(54.0)
47
(54.7)
0.974
(0.484–1.961)
0.941
S ess
(GHQ12)a20
(40.0)
43
(50.0)
0.667
(0.329–1.351)
0.259
S ess
(MBI)b15
(30.0)
37
(43.0)
0.568
(0.271–1.190)
0.132
S ess
(combina ion
c i e ia)c20
(40.0) 41
(47.7) 0.732
(0.361–1.483) 0.386
B
(n
=
135)
Non- esponde s:
59
Responde s:
76
S ess
(in e iew)
31
(52.5)
43
(56.6)
0.850
(0.429–1.683)
0.640
S ess
(GHQ12)a24
(40.7)
39
(51.3)
0.651
(0.327–1.293)
0.219
S ess
(MBI)b22
(37.3)
30
(39.5)
0.912
(0.453–1.836)
0.796
S ess
(combina ion
o
c i e ia)c24
(40.7)
37
(48.7)
0.723
(0.364–1.437)
0.354
OR
–
odds
a io;
95%
CI
–
95%
confidence
in e al.
aGene al
Heal h
Ques ionnai e
(GHQ12).
bMaslach
Bu nou
In en o y
(MBI).
cS ess
(in e iew
and
GHQ12)
o
s ess
(in e iew
and
MBI).
iangula ion
me hod
a
T0using
in e iews,
GHQ12 and
he
combina ion
o
he
h ee
me hods.
On
he
con a y,
we
did
no
find
any
s a is ically
significan
associa ion
be ween
he
o h-
e s
HAI
ab
i e
d op
g oups
a
T6and
he
p esence
o
ch onic
s ess
(Table
3).
Associa ion
be ween
o he
possible
con ounding
a iables
and
aemagglu ina ion-inhibi ion
ab
AH1 i e
d op
g oup
a
T6
Some
condi ions
ha
can
a ec
immuni y
could
ha e
been
possible
con ounding
ac o s,
when
we
conside ed
he
asso-
cia ion
be ween
s ess
and
he
HAI
ab
AH1 i e
d op
g oup
a
T6.
Using
he
Kolmogo o –Smi no
and
Shapi o–Wilk
es s,
we
ound
ha
he e
is
no
no mal
dis ibu ion
in
HAI
ab
AH1 i e
d op
g oup
a
T6and
in
no
change
in
HAI
ab
AH1 i e
a
T6 o
he
conside ed
con inuous
a iables
(p
<
0.001).
The e o e,
we
applied
he
Mann–Whi ney
es
o
compa e
hei
medians.
The
s a is ical
analyses
did
no
find
any
significan
di e -
ence
be ween
g oups
a
T6 o
he
a iables
(con inuous
and
dicho omous)
aken
in o
conside a ion
(Table
4).
Mul i a ia e
analysis
and
adjus ed
odds
a ios
o
s ess,
age
and
aemagglu ina ion-inhibi ion
ab
AH1 i es
a
T0
and
T1conside ing
aemagglu ina ion-inhibi ion
ab
AH1
i e
d op
g oup
a
T6
S ess
–
assessed
by
in e iew,
GHQ12 o
using
he
combina ion
o
he
h ee
me hods
–
was
he
exclusi e
a iable
associa ed
wi h
HAI
ab
AH1 i e
d op
g oup
a
T6,
bu
we
also
ook
he
age
a iable
in o
conside a ion
in
he
mul i a ia e
analysis.
Tha
op ion
was
made
because
age
is
a
s ong
ac o
influencing
immuni y
and,
in
he
simple
analysis,
he
median
di e ence
be ween
g oups
would
be
di e en
i
we
conside ed
a
confi-
dence
le el
o
90%
(ins ead
o
95%).
Fu he mo e,
Beye
and
colleagues
showed
ha
basal
HAI
ab
AH1 i es
influence
HAI
ab
AH1 i es
one
mon h
a e
Table
2
–
HAI
an ibodies
AH1,
AH3and
B
i es
a
T0in
non- esponde s
and
in
esponde s
AH1,
AH3and
B
a
T1.
HAI
an ibodies
a
T0Non- esponde s
a
T1Responde s
a
T1S a is ical
analysis
(Mann–Whi ney
es )
Md
(min–max)
Md
(min–max)
Md
di e ences
p
HAI
ab
AH1 i es
a
T0in
non- esponde s
AH1(n
=
45)
and
esponde s
AH1(n
=
90)
a
T1
640.0
(80–10,240)
20.0
(10–1280)
620.0
<0001
HAI
ab
AH3 i es
a
T0in
non- esponde s
AH3(n
=
50)
and
esponde s
AH3(n
=
86)
a
T1
160.0
(10–5120)
20.0
(10–1280)
140.0
<0001
HAI
ab
B
i es
a
T0in
non- esponde s
B
(n
=
59)
and
esponde s
B
(n
=
76)
a
T1
160.0
(20–10,240)
60.0
(10–640)
100.0
<0001
Md
-
median.

e
p
o
s
a
ú
d
e
p
ú
b
l
i
c
a
.
2
0
1
4;3
2(1):18–26
23
Table
3
–
S ess
in
HAI
an ibodies
i e
d op
g oup
and
in
no
change
in
HAI
Ab
i e
g oup
AH1,
AH3and
B
a
T6.
HAI
ab
g oups
a
T6Ch onic
s ess
assessmen
S ess
in
HAI
ab
i e
d op
g oup
a
T6
S ess
in
no
change
in
HAI
Ab
i e
g oup
a
T6
S a is ical
analysis
(Qui-squa e
es )
n
(%)
n
(%)
OR
(95%
CI)
p
AH1
(n
=
88)
HAI
ab
i e
d op
g oup:
57
No
change
in
HAI
ab
i e
g oup:
31
S ess
(in e iew) 36
(63.2) 10
(32.3)
3.600
(1.427–9.084)
0.006
S ess
(GHQ12)a33
(57.9)
11
(35.5)
2.500
(1.012–6.176)
0.045
S ess
(MBI)b25
(43.9)
10
(32.3)
1.641
(0.656–4.104)
0.288
S ess
(combina ion
o
c i e ia)c
34
(59.6)
7
(22.6)
5.068
(1.875–13.70)
0.001
AH3
(n
=
81)
HAI
ab
i e
d op
g oup:
48
No
change
in
HAI
ab
i e
g oup:
33
S ess
(in e iew)
25
(52.1)
21
(63.6)
0.621
(0.251–1.539)
0.302
S ess
(GHQ12)a26
(54.2)
(51.5)
1.112
(0.458–2.703)
0.814
S ess
(MBI)b20
(41.7)
16
(48.5)
0.759
(0.311–1.851)
0.544
S ess
(combina ion
o
c i e ia)c
23
(47.9)
18
(54.5)
0.767
(0.315–1.865)
0.558
B
(n
=
76)
HAI
ab
i e
d op
g oup:
51
No
change
in
HAI
ab
i e
g oup:
25
S ess
(in e iew)
26
(51.0)
17
(68.0)
0.489
(0.179–1.335)
0.160
S ess
(GHQ12)a27
(52.9)
12
(48.0)
1.219
(0.468–3.177)
0.686
S ess
(MBI)b17
(33.3)
13
(52.0)
0.462
(0.174–1.226)
0.118
S ess
(combina ion
o
c i e ia)c
22
(43.1)
15
(60.0)
0.506
(0.191–1.339)
0.167
OR
–
odds
a io;
95%
CI
–
95%
confidence
in e al.
aGene al
Heal h
Ques ionnai e
(GHQ12).
bMaslach
Bu nou
In en o y
(MBI).
cS ess
(in e iew
and
GHQ12)
o
s ess
(in e iew
and
MBI).
Table
4
–
Va iables
dis ibu ion
(s ess
no
included)
in
HAI
ab
AH1 i e
d op
g oup
a
T6and
in
no
change
in
HAI
ab
AH1
i e
g oup
AH1a
T6.
Va iables HAI
ab
AH1 i e
d op
g oup
a
T6(n
=
57)
No
change
in
HAI
ab
AH1 i e
g oup
a
T6
(n
=
31)
S a is ical
analysis
(Fishe
es
o
Qui-squa e
es
o
Mann–Whi ney
es )
n
(%)
n
(%)
OR
(95%
CI)
p
Male
gende
5
(8.8)
7
(22.6)
0.330
(0.095–1.145)
0.103a
Caucasian
53
(93.0)
31
(100)
0.631
(0.536–0.743)
0.293a
Shi
wo k
35
(61.4)
23
(74.2)
0.553
(0.211–1.453)
0.250a
Daily
sleep
hou s
<
7
20
(35.1)
8
(25.8)
0.643
(0.244–1.699)
0.372b
Smoke s
10
(17.5)
9
(29.0)
0.520
(0.185–1.461)
0.211b
Vi amin
supplemen s
10
(17.5)
4
(12.9)
1.436
(0.410–5.025)
0.762a
Fish
oil
consump ion
0
(0.0)
0
(0.0)
Daily
consump ion
o
yogu s
27
(47.4)
15
(48.4)
0.960
(0.400–2.304)
0.927b
No
egula
physical
ac i i y
29
(50.9)
11
(35.5)
1.883
(0.765–4.634)
0.166b
Pas
influenza
accine
17
(29.8)
12
(38.7)
0.673
(0.268–1.687)
0.397b
Influenza
accine
a
2006
14
(24.6)
11
(35.5)
0.592
(0.229–1.533)
0.278b
HAI
ab
AH1a
T0≥
40 25
(43.9)
17
(54.8)
0.643
(0.267–1.551)
0.325b
Va iables
HAI
ab
AH1 i e
d op
g oup
a
T6(n
=
57)
No
change
in
HAI
ab
AH1 i e
g oup
a
T6
(n
=
31)
S a is ical
analysis
(Fishe
es
o
Qui-squa e
es
o
Mann–Whi ney
es )
Md
(min–max)
Md
(min–max)
Md
di e ences
p
Age
31.0
(23.0–63.0)
26.0
(22.0–56.0)
5.0
0.072c
Body
index
mass
22.7
(17.7–37.8)
22.0
(18.0–37.5)
0.7
0.793c
HAI
ab
AH1 i es
a
T020.0
(10–640)
40.0
(10–1280)
−20.0
0.276c
HAI
ab
AH1
i es
a
T11280.0
(40–20,480)
1280.0
(160–20,480)
0.0
0.265c
Md
–
median.
aFishe
es .
bQui
Squa e
es .
cMann–Whi ney
es .
24
e
p
o
s
a
ú
d
e
p
ú
b
l
i
c
a
.
2
0
1
4;3
2(1):18–26
Table
5
–
Mul i a ied
analysis
(mul iple
logis ic
eg ession)
o
s ess
(assessed
by
iangula ion
me hod
using
GHQ12,
using
in e iew
and
using
he
combina ion
o
he
h ee
me hods)
in
HAI
ab
AH1 i e
d op
g oup
a
T6conside ing
age,
HAI
ab
AH1 i es
a
T0and
a
T1.
Ch onic
s ess
assessmen
Conside ed
a iables
in
mul i a ied
analysis
S a is ical
analysis
(mul iple
logis ic
eg ession)
Adjus ed
OR
(95%
CI)
p
GHQ12 a
Age
1.038
(0.989–1.089)
0.134
S ess
2.733
(1.039–7.186)
0.042
HAI
ab
AH1a
T00.998
(0.995–1.000)
0.100
HAI
ab
AH1a
T11.000
(1.000–1.000)
0.793
In e iew
Age 1.043
(0.994–1.094) 0.083
S ess
3.643
(1.371–9.684)
0.010
HAI
ab
AH1a
T00.999
(0.996–1.001)
0.236
HAI
ab
AH1a
T11.000
(1.000–1.000)
0.987
Combina ion
o
c i e iab
Age
1.044
(0.994–1.096)
0.087
S ess
5.223
(1.828–14.924)
0.002
HAI
ab
AH1a
T00.999
(0.996–1.001)
0.255
HAI
ab
AH1a
T11.000
(1.000–1.000)
0.892
Adjus ed
OR
–
adjus ed
odds
a io;
95%
CI
–
95%
confidence
in e al.
aGene al
Heal h
Ques ionnai e
(GHQ12).
bS ess
(in e iew
and
GHQ12)
o
s ess
(in e iew
and
MBI).
accina ion.28 The e o e,
we
also
conside ed
HAI
ab
AH1 i es
a
T0and
T1in
he
mul i a ia e
analysis.
We
ound
ha
s ess,
assessed
by
iangula ion
me hod
using
GHQ12,
using
in e iew
and
using
he
combina ion
o
he
h ee
me hods,
main ained
he
associa ion
wi h
HAI
ab
AH1 i e
d op
g oup
a
T6.
The
associa ion
be ween
HAI
ab
AH1 i e
d op
g oup
a
T6and
he
o he s
a iables
did
no
e eal
any
s a is ical
significance
(Table
5).
When
we
assessed
s ess
by
iangula ion
me hod
using
GHQ12,
he
model
was
s a is ically
significan
(p
<
0.029)
and
sui able,
gi en
ha
null
hypo hesis
was
no
ejec ed
in
he
Hosme –Lemeshow
es
(p
<
0.106).
The
model
showed
a
alid-
i y
a e
o
65.9.
When
we
assessed
s ess
by
iangula ion
me hod
using
in e iew,
he
model
was
s a is ically
significan
(p
<
0.009)
and
sui able,
gi en
ha
null
hypo hesis
was
no
ejec ed
in
he
Hosme –Lemeshow
es
(p
<
0.761).
The
model
showed
a
alid-
i y
a e
o
71.6.
When
we
assessed
s ess
by
iangula ion
me hod
using
he
combina ion
o
he
h ee
me hods,
he
model
was
s a-
is ically
significan
(p
<
0.002)
and
sui able,
gi en
ha
null
hypo hesis
was
no
ejec ed
in
he
Hosme –Lemeshow
es
(p
<
0.679).
The
model
showed
a
alidi y
a e
o
73.9.
Discussion
and
conclusions
When
human
beings
a e
exposed
o
ch onic
s esso s,
hey
may
espond
o
hem
wi h
neu oendoc ine
changes
ha
include
he
elease
o
neu opep ides,
monoamines
and
ho -
mones.
Mos
o
hose
subs ances
a e
able
o
change
he
immune
cells
beha iou .29
Psychological
ch onic
s ess
can
change
an ibody
(ab)
p o-
duc ion
and
kine ics
a e
accina ion,
in
pa icula
a e
he
influenza
accine
is
gi en
o
elde ly
people
who
ake
ca e
o
spouses
wi h
demen ia.9–12
Va ious
s udies
o
elde ly
people
ha e
ound
an
asso-
cia ion
be ween
exposu e
o
a
long- e m
s esso
(such
as
demen ia
spouse
ca egi ing)
and
a
small
p opo ion
o
hem
who
eached
a
leas
ab
HAI
i es
ha
we e
ou old
wha
hey
had
be o e
flu
accina ion,
assessed
one
mon h
a e
accina ion.13–15 Be ea emen
and
ma iage
seem
o
be
asso-
cia ed
wi h
an ibody
esponse
o
influenza
accina ion
in
he
elde ly
as
well.17
In
ou
s udy,
as
in
some
o he
s udies
in ol ing
young
adul s,18,23–25 we
did
no
find
any
associa ion
be ween
he
p esence
o
ch onic
s ess
in
nu ses
and
he
p opo ion
o
hem
ha
each
a
leas
ou
imes
he
ab
HAI
i e
le els
hey
had
be o e
flu
accina ion.
On
he
con a y,
o he
s udies
ha e
ound
an
associa ion
among
pe cei ed
dis ess,19 li e
e en s,20
neu o icism21 and
loneliness22 and
he
immune
esponse
o
flu
accina ion,
assessed
one
mon h
o
fi e
weeks
a e .
I
is
possible
ha
me hodological
issues
can
explain
dis-
c epancies
in
esul s
e ified
in
s udies
wi h
younge
g oups,
such
as:
(1)
di e en
ways
o
cha ac e ising
independen
a i-
ables;
(2)
samples
wi h
di e ing
demog aphic
cha ac e is ics
and
dimensions;
(3)
di e ing
his o ies
o
flu
i us
exposu e.
Wi h
espec
o
he
la e
issue,
ou
s udy
ound
ha
non-
esponde s
had
significan ly
highe
ab
HAI
AH1N1,
AH3N2and
B
i es
a
T0 han
esponde
g oups.
The e o e,
as
pos ula ed
by
Beye
and
colleagues,28 ab
HAI
i es
a
T0,
showed
o
be
an
impo an
con ounding
a iable
when
s udying
he
ela ion-
ship
be ween
s ess
and
immune
esponse
o
flu
accine
one
mon h
a e
accina ion
and
mus
be
conside ed.
Ne e heless,
we
ound
an
associa ion
be ween
he
p es-
ence
o
ch onic
s ess
(measu ed
in
h ee
di e en
ways)
and
a
d op
in
ab
HAI
(AH1N1)
a
T6.
O he
s udies
also
ound
an
asso-
cia ion
be ween
dis ess,19,25 li e
e en s,20 li e
e en s
weighed
wi h
pe cei ed
s ess,23 neu o icism,21 o
loneliness22 and
a
d op
in
ab
HAI
ou
o
six
mon hs
a e
accina ion.
Those
associa ions
we e
ound
o
a
leas
one
s ain
composing
he
flu
accine.
e
p
o
s
a
ú
d
e
p
ú
b
l
i
c
a
.
2
0
1
4;3
2(1):18–26
25
Ou
s udy
ound
a
la ge
p opo ion
o
nu ses
wi h
ch onic
s ess
in
he
HAI
ab
AH1 i e
d op
g oup
a
T6,
as
compa ed
o
he
no
change
in
HAI
Ab
AH1 i e
g oup
a
T6,
when
we
measu ed
s ess
by
iangula ion
me hod,
using
in e iew
o
GHQ12 o
assess
pe cei ed
s ess,
and
using
he
combina ion
o
he
h ee
me hods
(as
desc ibed
in
he
me hods
sec ion).
We
did
no
find
any
s a is ically
significan
associa ion
when
we
assessed
he
p esence
o
s ess
by
he
iangula ion
me hod
bu
using
he
MBI
exhaus ion
scale
o
measu e
pe cei ed
s ess.
A
possible
explana ion
is
he
ac
ha
he
MBI
exhaus-
ion
scale
measu es
specifically
wo k- ela ed
s ess
and
he
possible
immunologic
epe cussions
o
ch onic
s ess
seem
o
be
independen
o
he
s ess
sou ce.
As
desc ibed
in
o he
s udies,19–23,25 he
associa ion
be ween
s ess
and
a
d op
in
ab
HAI
a
T6did
no
occu
o
all
he
accine
s ains
componen s.
S ain
no el y
can
be
an
impo an
ac o
in
ha
analy-
sis,
as
a gued
by
o he
au ho s.15,20 P essman
and
colleagues,
o
example,
only
ound
an
associa ion
be ween
s ess
and
a
d op
in
HAI
ab,
ou
mon hs
a e
accina ion,
o
a
s ain
ha
was
no
included
in
p e ious
accina ions
he
pa ici-
pan s
ecei ed.25 In
ou
s udy,
he
exclusi e
s ain
ha
was
no
included
in
flu
accines
in
he
h ee
p eceding
yea s
was
he
A(H1N1)
s ain.
In
Po ugal
he
p edominan
ci cula ing
s ains
wi h
high
flu
ac i i y
since
1990
ha e
been
A(H3N2)
and
B.
F om
1990
o
he
beginning
o
he
s udy,
he
A(H1N1)
s ain
was
only
p e-
dominan
in
2005,
simul aneously
wi h
s ain
B,
and
2005
was
a
yea
wi h
e y
low
flu
ac i i y.30 We
also
know
ha
A
s ains
unde go
mo e
d i
mu a ions
han
B
s ains,31 so
his
can
con-
ibu e
o
hei
being
a
ela i e
no el y
o
he
pa icipan s’
immune
sys em.
Finally,
in
ou
s udy,
he
A(H1N1)
influenza
s ain
p o ed
o
be
he
mos
immunogenic
one,
showing
a
ise
in
he
HAI
Ab
i e
geome ic
mean
o
11.1.
A
(H3N2)
and
B
s ains
showed
ises
o
6.2
and
4.6
imes,
espec i ely,
be ween
T0and
T1.
I
is
possible
ha
he
bes
immunogenici y
obse ed
o
he
A
(H1N1)
s ain
was
ela ed
wi h
he
ac
ha
some
pa ici-
pan s
had
had
a
p ima y
in ec ion
wi h
an
A
(H1N1)
s ain,
so
he
esponse
o
A
(H1N1)
an igens
ha e
been
mo e
obus
in
hem.32 Tha
could
be
a
ac o
ha
may
influence
he
de ec-
ion
o
he
associa ion
be ween
s ess
and
d ops
in
HAI
ab
a e
a
pe iod
o
ime.
Gi en
ha
ou
sample
was
no
a
andomised
sample
because
i
depended
on
nu ses
olun a ily
being
accina ed
and
pa icipa ing
in
he
s udy,
we
analysed
dis ibu ion
di -
e ences
o
some
a iables
in
he
HAI
ab
AH1 i e
d op
g oup
a
T6and
he
no
change
in
HAI
Ab
AH1 i e
g oup
a
T6 ha
a e
no
included
in
d op
ou
c i e ia.
As
he e
a e
a
lo
o
a iables
o
which
we
do
no
ye
know
i
hey
can
influence
immu-
ni y,
we
s udied
hose
ha
a e
mos
e e ed
o
in
he
ele an
li e a u e.33
We
did
no
find
any
di e ences
in
he
dis ibu ion
o
he
s udied
a iables
in
he
wo
g oups
a
T6.
Ne e heless,
we
decided
o
include
ab
AH1 i es
a
T0,
ab
AH1 i es
a
T1and
age
in
mul iple
logis ic
eg ession.
The
eason
o
including
he
fi s
wo
a iables
was
he
s ong
sugges ion
in
li e a u e
ha
hey
can
influence
ab
i es
a e
accina ion
(immune
esponse),28 e en
hough
we
ound
no
e e ences
o
he
influence
hey
ha e
on
a
d op
in
i es
six
mon hs
a e
flu
accina ion.
Age
is
s ongly
ela ed
wi h
immuni y33 bu
we
did
no
find
any
di e ence
in
e ms
o
age
be ween
he
wo
g oups
conside ed
a
T6a
he
significance
le el
we
con-
side ed
(5%).
I
we
conside ed
a
significance
le el
o
10%
he
esul
would
be
di e en .
Hence,
we
also
included
age
in
he
mul i a ia e
analysis.
A e
he
mul i a ia e
analysis,
we
s ill
ound
an
associ-
a ion
wi h
s a is ical
significance
be ween
he
p esence
o
ch onic
s ess
and
he
HAI
ab
AH1 i e
d op
g oup
a
T6,
when
we
assessed
s ess
in
h ee
di e en
ways,
all
o
hem
using
he
iangula ion
me hod,
as
sugges ed
by
Cox
and
colleagues,
as
a
good
way
o
measu ing
s ess.26 The e o e,
he
ela ion-
ship
ha
we
ound
be ween
ch onic
s ess
and
a
d op
in
HAI
ab
a
T6suppo s
he
hesis
ha
s ess
can
nega i ely
influence
HAI
ab
i es
some
mon hs
a e
flu
accina ion
e en
in
people
in
adul s
unde
he
age
o
60.
As
we
could
no ice,
his
is
he
fi s
s udy
assessing
he
associa ion
be ween
ch onic
s ess
and
immune
esponse
o
influenza
accine
in
heal hca e
wo ke s,
who
is
an
impo an
a ge
g oup
o
influenza
accine.
The e-
o e,
in
an
occupa ional
heal h
en i onmen ,
i
is
easonable
o
conside
he
possible
in e e ence
o
ch onic
s ess
wi h
ab
i es
when
we
implemen
accina ion
p og ammes
o
p e en
biological
occupa ional
isks.
Funding
Au o idade
pa a
as
Condic¸ões
de
T abalho
(ACT)
unded
he
labo a o ial
e alua ion
o
he
s udy.
Conflic s
o
in e es
The
au ho s
ha e
no
conflic s
o
in e es
o
decla e.
e
e
e
n
c
e
s
1.
Chang
EM,
Daly
JW,
Hancock
KM,
Bidewell
J,
Johnson
A,
Lambe
VA,
e
al.
The
ela ionships
among
wo kplace
s esso s,
coping
me hods,
demog aphic
cha ac e is ics
and
heal h
in
Aus alian
nu ses.
J
P o
Nu s.
2006;22:30–8.
2.
G aham
IW,
And ews
T,
Cla ck
L.
Mu ual
su e ing:
A
nu se’s
s o y
o
ca ing
o
he
li ing
as
hey
a e
dying.
In
J
Nu s
P ac .
2005;11:277–85.
3.
Xianyu
Y,
Lambe
VA.
In es iga ion
o
he
ela ionships
among
wo kplace
s esso s,
ways
o
coping
and
he
men al
heal h
o
Chinese
head
nu ses.
Nu s
Heal h
Sci.
2006;8:147–55.
4.
Linds om
K.
Wo k
o ganiza ion
and
well-being
o
Finnish
heal h
ca e
pe sonnel.
Scand
J
Wo k
En i on
Heal h.
1992;18:90–3.
5.
Schau eli
WB.
Bu nou .
In:
Fi h-Cozens
J,
Payne
RL,
edi o s.
S ess
in
heal h
p o essionals.
Chiches e :
John
Wiley
&
Sons;
1999.
p.
17–32.
6.
Wol gang
AP.
Job
s ess
in
he
heal h
p o essions:
A
s udy
o
physicians,
nu ses
and
pha macis s.
Beha
Med.
1988;14:43–7.
7.
López-Cas illo
J,
Gu pegui
M,
Ayuso-Ma eos
JL,
Luna
JD,
Ca ala
J.
Emo ional
dis ess
and
occupa ional
bu nou
in
heal h
ca e
p o essionals
se ing
HIV-in ec ed
pa ien s:
A
compa ison
wi h
oncology
and
in e nal
medicine
se ices.
Psycho he
Psychosom.
1999;68:348–56.
8.
Hun
M.
Vi ology:
Influenza
i us:
O homyxo i us.
In:
Hun
RC,
edi o .
Mic obiology
and
immunology
online.
Chap e
26
e
p
o
s
a
ú
d
e
p
ú
b
l
i
c
a
.
2
0
1
4;3
2(1):18–26
hi een
[In e ne ].
Columbia,
SC:
School
o
Medicine,
Uni e si y
o
Sou h
Ca olina;
2011.
A ailable
om:
h p://www.mic obiologybook.o g/mhun /flu.h m
[ci ed
12.07.11].
9.
Sege s om
SC,
Mille
GE.
Psychological
s ess
and
he
human
immune
sys em:
A
me a-analy ic
s udy
o
30
yea s
o
inqui y.
Psychol
Bull.
2004;130:601–30.
10.
Bu ns
VE.
S ess
and
an ibody
esponse
o
accina ion:
Implica ions
o
animal
s udies
o
human
clinical
esea ch.
Expe
Re
Vaccines.
2004;3:141–9.
11.
Bu ns
VE,
Ca ol
D,
Ring
C,
D ayson
M.
An ibody
esponse
o
accina ion
and
psychosocial
s ess
in
humans:
Rela ionships
and
mechanisms.
Vaccine.
2003;21:
2523–34.
12.
Cohen
S,
Mille
GE,
Rabin
BS.
Psychological
s ess
and
an ibody
esponse
o
immuniza ion:
A
c i ical
e iew
o
he
human
li e a u e.
Psychosom
Med.
2001;63:7–18.
13.
Kiecol -Glase
JK,
Glase
R,
G a ens ein
S,
Mala key
WB,
She idan
J.
Ch onic
s ess
al e s
he
immune
esponse
o
influenza
i us
accine
in
olde
adul s.
P oc
Na l
Acad
Sci
U
S
A.
1996;93:3043–7.
14.
Glase
R,
Kiecol -Glase
JK,
Mala key
W,
She idan
JF.
The
influence
o
psychological
s ess
on
he
immune
esponse
o
accines.
Ann
N
Y
Acad
Sci.
1998;840:649–55.
15.
Vedha a
K,
Cox
NK,
Wilcock
GK,
Pe ks
P,
Hun
M,
Ande son
S,
e
al.
Ch onic
s ess
in
elde ly
ca ee s
o
demen ia
pa ien s
and
an ibody
esponse
o
influenza
accina ion.
Lance .
1999;353:627–31.
16.
Vedha a
K,
Benne
PD,
Cla k
S,
Ligh man
SL,
Shaw
S,
Pe ks
P,
e
al.
Enhancemen
o
an ibody
esponses
o
accina ion
in
he
elde ly
ollowing
a
cogni i e-beha iou al
s ess
managemen
in e en ion.
Psycho he
Psychosom.
2003;72:245–52.
17.
Philips
AC,
Ca ol
D,
Bu ns
VE,
Ring
C,
Macleod
J,
D ayson
M.
Be ea emen
and
ma iage
a e
associa ed
wi h
an ibody
esponse
o
influenza
accina ion
in
he
elde ly.
B ain
Beha
Immun.
2006;20:279–89.
18.
Vedha a
K,
McDe mo
MP,
E ans
TG,
T eano
JJ,
Plumme
S,
Tallon
D,
e
al.
Ch onic
s ess
in
nonelde ly
ca egi e s:
Psychological,
endoc ine
and
immune
implica ions.
J
Psychosom
Res.
2002;53:1153–61.
19.
Mille
GE,
Cohen
S,
P essman
S,
Ba kin
A,
Rabin
BS,
T eano
JJ.
Psychological
s ess
and
an ibody
esponse
o
influenza
accina ion:
When
is
he
c i ical
pe iod
o
s ess
and
how
does
i
ge
inside
he
body?
Psychosom
Med.
2004;66:
215–23.
20.
Philips
AC,
Bu ns
VE,
Ca ol
D,
Ring
C,
D ayson
M.
The
associa ion
be ween
li e
e en s,
social
suppo
and
an ibody
s a us
ollowing
hymus-dependen
and
hymus-independen
accina ions
in
heal hy
young
adul s.
B ain
Beha
Immun.
2005;19:325–33.
21.
Philips
AC,
Ca ol
D,
Bu ns
VE,
D ayson
M.
Neu o icism,
co isol
eac i i y
and
an ibody
esponse
o
accina ion.
Psychophysiology.
2005;42:232–8.
22.
P essman
SD,
Cohen
S,
Mille
GE,
Ba kin
A,
Rabin
BS,
T eano
JJ.
Loneliness,
social
ne wo k
size
and
immune
esponse
o
influenza
accina ion
in
college
eshmen.
Heal h
Psychol.
2005;24:297–306.
23.
Bu ns
VE,
Ca ol
D,
D ayson
M,
Whi ham
M,
Ring
C.
Li e
e en s,
pe cei ed
s ess
and
an ibody
esponse
o
influenza
accina ion
in
young
heal hy
adul s.
J
Psychosom
Res.
2003;55:569–72.
24.
La son
MR,
T eano
JJ,
Ade
R.
Psychosocial
influences
on
esponses
o
educed
and
ull-dose
i alen
inac i a ed
accine.
Psychosom
Med.
2002;64:113.
25.
P essman
S,
Cohen
S,
Mille
G,
Rabin
B.
S ess
and
an ibody
esponse
o
influenza
immuniza ion
in
college
eshman.
B ain
Beha
Immun.
2002;16:208
[abs ac ].
26.
Cox
T,
G i fi hs
A,
Rial-González
E.
Resea ch
on
wo k- ela ed
s ess.
Luxembou g:
O fice
o
O ficial
Publica ions
o
he
Eu opean
Communi ies;
2000.
27.
Wo ld
Heal h
O ganiza ion.
Iden ifica ion
o
isola es
by
hemagglu ina ion
inhibi ion.
In:
WHO,
edi o .
WHO
animal
manual:
Diagnosis
and
su eillance.
Gene a:
Depa men
o
Communicable
Disease
Su eillance
and
Response;
2002.
p.
28–36.
28.
Beye
WE,
Palache
AM,
Sp enge
MJ,
Hend iksen
E,
Tukke
JJ,
Da ioli
R,
e
al.
E ec s
o
epea ed
annual
influenza
accina ion
se o- esponse
in
young
and
elde ly
adul s.
Vaccine.
1996;14:1331–9.
29.
Cohen
N,
Kinney
KS.
Explo ing
he
phylogene ic
his o y
o
neu al-immune
sys em
in e ac ions:
An
upda e.
In:
Ade
R,
edi o .
Psychoneu oimmunology.
London:
Else ie
Academic
P ess;
2007.
p.
1–38.
30.
Rebelo-de-And ade
H,
Falcão
JM,
C espo
N.
G ipe
sazonal
e
pandémica.
P og ama
de
In e enc¸ão
do
INSA.
Lisboa:
Ins i u o
Nacional
de
Saúde;
2006.
31.
USA.
CDC
(Cen e s
o
Diseases
Con ol
and
P e en ion).
P e en ion
and
con ol
o
influenza:
Recommenda ions
o
he
Ad iso y
Commi ee
on
Immuniza ion
P ac ices
(ACIP).
MMWR.
2007;56RR-6:1–54.
32.
Pe ei a
MS.
Global
su eillance
o
influenza.
B
Med
Bull.
1979;35:9–14.
33.
Lo e en
HV,
Ams e dam
JG,
Vandeb iel
RJ,
Kimman
TG,
Rumke
HC,
S ee enbe g
PS,
e
al.
Vaccine-induced
an ibody
esponses
as
pa ame e s
o
he
influence
o
endogenous
and
en i onmen al
ac o s.
En i on
Heal h
Pe spec .
2001;109:757–64.