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African swine fever (ASF), the pig health challenge of the century

Author: Martins, Carlos,Boinas, F. S.,Iacolina, Laura,Gavier-Widén, Dolores,Ruiz-Fons, Francisco
Publisher: Wageningen Academic Publishers
DOI: http://dx.doi.org/10.13039/501100000781
Source: https://digital.csic.es/bitstream/10261/264672/1/ASFcentury.pdf
Vi agenes in a ian biology and poul y heal h 11
Lau a Iacolina e al. (eds.) Unde s anding and comba ing A ican swine e e
DOI 10.3920/978-90-8686-910-7_1, © C. Ma ins e al., 2021 OPEN ACCESS
This publica ion is based upon wo k om COST Ac ion CA15116, ASF-STOP,
suppo ed by COST (Eu opean Coope a ion in Science and Technology).
www.cos .eu
Funded by he Ho izon 2020 F amewo k P og amme
o he Eu opean Union
1. A ican swine e e (ASF), he pig heal h
challenge o he cen u y
C. Ma ins1*, F.S. Boinas1, L. Iacolina2,3, F. Ruiz-Fons4 and D. Ga ie -Widén5,6
1CIISA – Cen o de In es igação In e disciplina em Sanidade Animal, Faculdade de Medicina Ve e iná ia, Uni e sidade de Lisboa,
A enida da Uni e sidade Técnica, 1300-477 Lisboa, Po ugal; 2Depa men o Chemis y and Bioscience, Aalbo g Uni e si y,
F ede ik Baje s Vej 7H, 9220 Aalbo g, Denma k; 3Facul y o Ma hema ics, Na u al Sciences and In o ma ion Technologies, Uni e si y
o P imo ska, Glagoljaška 8, SI-6000 Kope , Slo enia; 4Heal h & Bio echnology (SaBio) G oup, Spanish Game and Wildli e Resea ch
Ins i u e (IREC; CSIC-UCLM-JCCM), Ronda de Toledo 12, 13071 Ciudad Real, Spain; 5Depa men o Pa hology and Wildli e Diseases,
Na ional Ve e ina y Ins i u e (SVA), 751 89, Uppsala, Sweden; 6Depa men o Biomedical Sciences and Ve e ina y Public Heal h,
Swedish Uni e si y o Ag icul u al Sciences (SLU), Box 7028, 750 07 Uppsala, Sweden; cma ins@ m .ulisboa.p
Abs ac
Mo e han one hund ed yea s ago A ican swine e e (ASF) was i s diagnosed in Kenya. Since
hen, di e se app oaches ha e been applied o he s udy o he causa i e i us, he sole membe
o he amily As a i idae, aimed a cha ac e ising i s p ope ies, genome o ganisa ion and
eplica ion, i s an igenic and biological p ope ies as well as o de elop ea men and a accine.
The disease e ol ed and has pe sis ed in A ica in a syl a ic cycle in ol ing wild suids and so
icks o a long ime, bu was in oduced, usually h ough con amina ed was e ood, in o o he
egions on mul iple occasions since 1957. The mos ecen in oduc ion, in o Geo gia in 2007,
esul ed in he sp ead o he disease o he Eu opean Union in 2014 and o he es ablishmen o
an in e na ional and mul idisciplina y ne wo k o scien is s unded by he Eu opean Coope a ion
in Science and Technology (COST) wo yea s la e . The ne wo k included a b oad a ie y o
scien i ic ields, animal heal h and ood sa e y au ho i ies, hun ing associa ions, wildli e manage s
and ood and li es ock indus ies wi h he goal o inc easing p epa edness and a emp ing o s op
ASF sp ead. This book ep esen s he summa y o he collec i e and in eg a ed wo k o almos
300 dedica ed pa icipan s in ackling he complex challenge posed by ASF. He e we summa ise
he s a e-o - he-a knowledge on his le hal disease, wi h a ocus on he Eu opean si ua ion, and
iden i y a eas ha s ill need o be explo ed.
Keywo ds: A ican swine e e , his o y, mul idisciplina y, Eu ope
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C. Ma ins e al.
12 Unde s anding and comba ing A ican swine e e
1.1 Whe e ASF-STOP comes om
Mo e han one hund ed yea s ago, R. Eus ace Mon gome y diagnosed o he i s ime, in Kenya,
he occu ence o a swine disease cha ac e ised by clinical and pa hological ea u es simila bu no
ela ed o classical swine e e (CSF) o hog chole a. His obse a ions and s udies, de eloped om
1910 up o 1917, showed ele an aspec s o he ‘Eas A ican swine e e ’ now known as A ican
swine e e (ASF) (Mon gome y, 1921). The au ho ’s indings a e s ill conside ed o be pilla s o
he knowledge a ained since hen on his disease, ha cu en ly in lic s ala ming ou b eaks wi h
de as a ing economic and social consequences in nume ous coun ies in A ica, Eu ope, Asia
and Oceania. Hund eds o esea che s and specialis s in di e en ields o knowledge, o p i a e
and public Na ional and In e na ional ins i u ions, ha e p oduced, along he yea s, coun less
documen s and scien i ic pape s dedica ed o explo e and deepen key aspec s on in ica e de ails
o he i us biology, disease main enance and dissemina ion, complex i al-hos in e ac ions,
s a egies o p e en and con ol disease ou b eaks and dissemina ion, and e o s o de elop sa e
and success ul accines. Recen e iews, including he chap e s o his book, ully co e di e en
aspec s o ASF and i would be supe luous o desc ibe ac s al eady a ailable o he likely al eady
in o med eade s. Thus, he main g ound-b eaking con ibu ions ha ha e p o ided new insigh s
in o he cu en knowledge on ASF a e p esen ed he e, o ein o ce s a egies owa ds p e en ion
and con ol o ASF.
Since Mon gome y’s indings, A ican swine e e i us (ASFV) has been s udied h ough di e se
app oaches aiming a cha ac e ising i s s uc u al and physicochemical p ope ies, genome
o ganisa ion and eplica ion, as well as i s an igenic and biological p ope ies. This complex
i us is a la ge double s anded DNA i us (170-190 kb) ha encodes mo e han 150 open
eading ames (ORFs), depending on he i us isola e. I is he only known DNA a bo i us and
he sole membe o he amily As a i idae, classi ied in o he Nucleocy oplasmic La ge DNA
Vi uses supe amily (Takama su e al., 2011). The i us in ec s all membe s o he Suidae amily
and i is main ained in di e en epidemiological cycles ela ed o dis inc ecosys ems. I was
diagnosed in A ica o he i s ime in 1910, when occu ence o ASF ou b eaks was ela ed o
he p esence o wa hogs (Phacochoe us sp.) and bush pigs (Po amochoe us sp.), bo h shown o
su i e expe imen al inocula ions wi h he causa i e i us wi hou mani es ing clinical signs.
Howe e , hei blood collec ed up o i e o se en days pos inocula ion was in ec ious and caused
ASF expe imen ally in domes ic pigs. The in ec ed wild suids did no , howe e , appea capable
o dissemina ing he i us by con ac , u ine, and aeces al hough he conside ed possible he
in ol emen o an a ho opod ec o , and was able o exclude leas and lice (Mon gome y, 1921).
Many yea s la e , in he 1960s, when ASF was sp eading in Eu ope, Sanchez Bo ija ound ha
ASFV in ec ed so icks (O ni hodo os e a icus), collec ed in pig s ies, we e ac ing as he
biological ec o s o ASFV in Spain (Sanchez-Bo ija, 1963). This inding opened new insigh s
ega ding he s udy o ASF epidemiology in A ica. Plow igh and colleagues (1969) desc ibed
he ea e ha so icks o he O ni hodo os mouba a complex we e ec o s and ese oi s o
ASFV in A ica. This new knowledge was u he pu sued by he iden i ica ion o he main ole o
O. mouba a icks in he ASF syl a ic epidemiological cycle. This cycle was shown o be connec ed
o common wa hogs (Phacochoe us a icanus) in Eas e n and Sou he n A ica (Pen i h e al.,
2004), he niche o he disease whose ae iological agen has been desc ibed as ha ing e ol ed o e
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1. ASF, he pig heal h challenge o he cen u y
Unde s anding and comba ing A ican swine e e 13
300 yea s wi h a ime o he mos ecen common ances o in he ea ly 18 h cen u y (Michaud
e al., 2013).
ASF has pe sis ed in A ica in a syl a ic cycle in ol ing wild suids and so icks, sp eading
h ough in ec ed O. mouba a icks o domes ic pig popula ions in which, a e wa ds, i eadily
sp eads h ough di ec and indi ec ansmission om in ec ed o heal hy pigs (Pen i h e al.,
2004). The disease was in oduced, p obably om Angola, o Po ugal in 1957 (Manso Ribei o e
al., 1958) in ASFV con amina ed was e ood om planes ha was ed as swill o pigs.
The disease was conside ed e adica ed he ollowing yea bu was again in oduced in 1960
(Manso Ribei o and Rosa Aze edo, 1961) and i emained endemic in Po ugal and Spain up o
he ea ly 1990s. Besides being main ained in he domes ic pig popula ions h ough di ec and
indi ec ansmission, i pe sis ed in popula ions o ee anging Ibe ian pigs, kep in p emises,
buil mos ly wi h s ones and adobe, du ing he nigh pe iods, allowing he es ablishmen o
he epidemiological cycle including he so icks O ni hodo os e a icus as biological ese oi s
(Caiado e al., 1988; Sanchez-Bo ija, 1963). In Eu ope, he dis ibu ion o his so ick is limi ed
o he Ibe ian pig ex ensi e p oduc ion a eas, in Cen al Spain and Sou hwes e n qua e o
Ibe ia (Mon ado/Po ugal and Dehesa/Spain), he las loca ions om which he disease was
e adica ed. The occu ence o a spo adic ou b eak, in 1999 in he Sou h o Po ugal, has been
epidemiologically connec ed wi h he p esence o O. e a icus in he pig p emises, as hese
a h opods a e e y esis an o as ing and may ha bou ac i e ASFV o up o 5 yea s (Boinas e
al., 2011). As a consequence, he epopula ion o he in es ed p emises in he a ea became limi ed
since i was only allowed based on he esul o a compulso y isk e alua ion. Mos o hem we e
depopula ed, which led o a signi ican dec ease in he p e alence o O. e a icus in mo e ecen
yea s (Wilson e al., 2013).
Al hough he epidemiological ole o he Eu asian wild boa (Sus sc o a) (WB) du ing he endemic
pe iod in Ibe ia was conside ed negligible, epidemiological su eys done a he ime showed ha
WB caused be ween 5-6% o he ASF ou b eaks (O das e al., 1983; Pe es elo-Viei a, 1993).
La e on, owa ds he end o he p e iously men ioned pe iod, se ological su eys in Po ugal
showed only 2.3% se op e alence in he hun ed WB popula ion in 1990 wi h no posi i es in 1992
(Commission o he Eu opean Communi ies-Di ec o a e Gene al o Ag icul u e, 1994). The
signi ican inc ease o WB in ecen yea s in he whole o Ibe ian Peninsula, and he inc ease o
ee- anging pig a ms, mainly in he Sou he n a eas, ce ainly would play a ele an ole in case
o ASF ein oduc ion.
The WB is known o be as suscep ible as he domes ic pig o ASF (Blome e al., 2013; Polo
Jo e and Sanchez-Bo ija, 1961), and is cu en ly conside ed o be he main d i e o a new
epidemiological cycle in disease main enance and sp ead since i eme ged in he Caucasus,
Russia, Eas e n Eu ope and Bal ic S a es (Gube i e al., 2020). This is u he desc ibed in de ail
la e in his book (Chap e s 8 and 9). In he I alian island o Sa dinia, ASF has been endemic since
1978, al hough e adica ion is likely o be achie ed soon. I s pe sis ence o mo e han 30 yea s has
equen ly been associa ed wi h he la ge popula ions o ee- ange ‘b ado’ pigs ha li e in he
moun ainous a ea in close con ac wi h WB, al hough WB is conside ed o mino impo ance in
his epidemiological scena io (Laddomada e al., 2019).
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C. Ma ins e al.
14 Unde s anding and comba ing A ican swine e e
S udies de eloped on he ole o se e al species o blood-sucking in e eb a es ound in pig
o wa hog habi a s ha e shown ha hey do no ansmi he i us a e ha ing an in ec ed
blood meal. Al hough no ac ing as biological ec o s in na u e like he a gasid icks, i was
expe imen ally shown ha s able lies (S omoxys calci ans) may ac as mechanical ec o s o
ASFV (Mello e al., 1987; Olesen e al., 2018).
In he e eb a e hos , he ae iological agen eplica es p e e en ially in monocy e and mac ophage
cells o he mononuclea phagocy ic sys em ( an Fu h and Cohn, 1968) and causes a ange o
synd omes and lesions, om pe acu e o ch onic and unappa en o ms o disease (Galla do e
al., 2015; Gómez-Villamandos e al., 2013). The clinical e olu ion o ASF is o en ela ed o he
di e se i ulence o he ae iological agen , which s ill emains o da e one o he mos in iguing
de ails o ASFV biology. When ASF was con ined o A ica and Ibe ian coun ies up o he ea ly
’60s, i al isola es in na u al occu ing ou b eaks we e shown o be highly i ulen , inducing
haemo hagic disease wi h mo ali y app oaching 100% o in ec ed animals (Manso Ribei o
e al., 1958; Mon gome y, 1921). Howe e , e en hough se e al au ho s claimed ha ASFV
i ulence would a enua e in ime a e he ini ial ou b eaks, possibly h ough i al adap a ion o
he hos (Plow igh e al., 1994), his was no he case. Fo example, in Po ugal highly i ulen
haemadso bing isola es (see Chap e 2) we e iden i ied up o he end o he endemic pe iod, o
e en when an isola ed and con olled ou b eak o disease occu ed in 1999 (Wilson e al., 2013).
Howe e , while ou b eaks caused by he highly i ulen haemadso bing isola e ASFV Lisbon 60
(L60) p e ailed, in ec ions wi h low i ulen non-haemadso bing isola es we e also iden i ied in
appa en ly heal hy pigs showing ch onic pulmona y lesions (Vigá io e al., 1974). This pa allel
occu ence o bo h low and highly i ulen ASFV isola es in na u e is no ully unde s ood.
Howe e , i is unlikely ha gene ic changes ha e na u ally occu ed in he highly i ulen L60 o
gi e o igin o he non-haemadso bing, low i ulen i us. The la e was ecen ly shown o ha e
signi ican gene ic di e ences when compa ed o he i ulen isola e (Po ugal e al., 2015). The
haemadso p ion e ec caused by some i us isola es, and demons a ed by Malmquis and Hay
(1960), was hough o a while o be a i ulence ma ke . Howe e , indings in A ica du ing
na u al occu ing ou b eaks ha e shown ha non-haemadso bing ASFV isola es can be bo h
i ulen and non- i ulen (Pini and Wagenaa , 1974; Thomson e al., 1979). The o igin o non-
haemadso bing isola es, showing di e en i ulence, is no clea ly unde s ood. I is accep ed
ha hey may occu in na u al condi ions, o igina ing om pa en al i us composed o a
he e ogeneous mix o di e en i uses, as demons a ed in i o by Pan and Hess (1984, 1985).
The de elopmen o molecula me hods has been a majo ad ance o s udy di e en aspec s
o ASFV biology. A landma k o ASFV genome cha ac e isa ion was achie ed h ough he
analysis o he comple e i al genome sequence o BA71V, an a i ulen ASFV isola e, adap ed
o g ow in Ve o cells (Yáñez e al., 1995). This wo k has p omp ed u he esea ch owa ds he
unc ional cha ac e isa ion o i al genes ha has been pu sued by di e en au ho s using o he
i al isola es. As ecen ly e iewed, ASFV encodes o a leas 150 p o eins and, so a , 38 o
hem a e associa ed wi h known o p edic ed unc ions in nucleo ide me abolism, ansc ip ion,
eplica ion and epai ; mo e han 24 p o eins a e in ol ed in i ion s uc u e and mo phogenesis,
and a leas 8 a e likely in ol ed in hos cell in e ac ions, al hough he unc ions o a la ge
numbe o ASFV encoded p o eins s ill emain unknown (Gaud eaul e al., 2020). Genome
sequencing has allowed molecula cha ac e isa ion o small conse ed DNA egions enabling
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1. ASF, he pig heal h challenge o he cen u y
Unde s anding and comba ing A ican swine e e 15
he de ec ion o o igin and aceabili y o ASFV du ing ou b eaks. The cu en app oach is based
on he analysis o he C- e minal end o gene B646L, encoding he majo p o ein p72 (Bas os
e al., 2003). Mo e ecen ly, his p ocedu e has been enhanced h ough he sequencing o he
Cen al Va iable Region (CVR) wi hin he B602L gene, o o he egions (e.g. E183L encoding p54
p o ein, CP204L encoding p30 p o ein), o dis inguish be ween geog aphically and empo ally
cons ained p72 geno ype i uses (Galla do e al., 2015). This app oach has allowed 24 di e en
p72 geno ypes o be iden i ied among he cu en ly known i us isola es. Ou o hese, geno ype
I is p edominan in Wes A ica and was he only one ound ou side A ica (Eu ope, Ame ica,
and he Ca ibbean) un il he in oduc ion o geno ype II om Eas A ica in o Geo gia in 2007.
This la e geno ype is he one cu en ly p esen in pa s o he Caucasus, Eu ope, he Russian
Fede a ion, Sou heas Asia and Oceania (Galla do e al., 2015; Gaud eaul e al., 2020). Al hough
impo an o de e mining epidemiological de ails o ASFV, he abo e-men ioned geno yping
does no co ela e o he i ulence o ASFV isola es as o en w ongly s a ed. The ques o he
iden i ica ion o ASFV i ulence ac o s o ma ke s has been pu sued o a long ime.
As men ioned abo e, ASFV i ulence was ini ially co ela ed o he haemadso p ion phenomenon
(Malmquis and Hay, 1960). P og essi ely, s udies ha e been de o ed o compa e genome
sequencing o di e en i us, o example h ough he use o isola es o di e en i ulence om
he same o igin (Po ugal e al., 2015). Such app oaches a e likely ele an o iden i y genes
ha may be o impo ance o be used in accine designing. De elopmen o e icien and sa e
accine(s) agains ASF is he ul ima e goal pu sued o mo e han one hund ed yea s (see Chap e
6) wi h he i s a emp s done by Mon gome y, who unsuccess ully ied o accina e domes ic
pigs wi h inac i a ed ASFV and who also ound ha an i-ASF se um did no neu alise he
i us (Mon gome y, 1921). Resea ch on accine de elopmen agains ASF has been ex ensi ely
epo ed by many au ho s co e ing, among o he s, de ails on he complexi y o he ASFV
pa icle, he la ge numbe o p o eins encoded by i s genome, he ASFV-hos in e ac ions,
he mechanisms o p o ec i e immuni y, and app oaches o accine de elopmen (A ias e
al., 2017). He ein, a ew aspec s will be emphasised ega ding i al-hos in e ac ions ha may
be conside ed as a cau iona y ou e when e alua ing accine design agains ASF. Fi s o all,
he p e e en ial eplica ion o ASFV in pig mac ophages is impo an . Nume ous s udies ha e
been conduc ed using pig mac ophages o cha ac e ise aspec s o i al modula ion o inna e
immune esponses po en ially ele an in i o, hus ideally o be used as ma ke s o es e icacy
o di e en accine models. Fo ins ance, in i o s udies ha e shown ha he i al in ec ion did
no al e he exp ession o Complemen Fixa ion (Fc) ecep o s o he abili y o media e an ibody
cellula cy o oxici y; in con as , phagocy osis, an ibody media ed phagocy osis and chemo axis
we e ab oga ed independen ly o he i ulence o ASFV isola e (Ma ins e al., 1987). Howe e ,
a low i ulen ASFV (ASFV/NH/P68 – NHV) was shown o induce an enhanced exp ession
and p oduc ion o ele an egula o y cy okines in e e on (IFN) (IFNalpha), umou nec osis
ac o (TNF) (TNF-α) and in e leukin (IL) (IL-12p40) on po cine mac ophages in i o, when
compa ed o he e ec o he i ulen ASFV Lisbon 60 (L60) (Gil e al., 2008). Mo e ecen ly,
o he s udies ha e sugges ed ha bo h L60 and NHV we e able o inhibi in e e on I (IFN I)
p oduc ion in mac ophages, h ough a mechanism no dependen on IRF3 modula ion (Po ugal
e al., 2018), while mac ophage esponses o NHV ha e been associa ed wi h enhanced sensi i i y
o ype I IFN and cy okine esponses om classically ac i a ed mac ophages (F anzoni e al.,
2020). Modula ion o cellula IFN esponses o in ec ion wi h a enua ed i us and induc ion o
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C. Ma ins e al.
16 Unde s anding and comba ing A ican swine e e
di e en p o ec i e immuni y has been demons a ed h ough dele ion o genes om mul igene
amilies (MGF) on a i ulen ASF isola e (Reis e al., 2016).
ASF e ol es equen ly in domes ic pigs as a con agious and usually acu e haemo hagic and
le hal disease, al hough some pigs may su i e, which is common when hey a e in ec ed wi h
low i ulen ASFV isola es al hough, in such cases, ch onic ype in ec ions may de elop (Galla do
e al., 2015; Lei ão e al., 2001). In gene al, pigs su i ing ASF a e esis an o challenge wi h
homologous o , in some cases, wi h closely ela ed i us isola es, sugges ing he p esence o a
no ye ully unde s ood e icien p o ec i e immuni y agains in ec ion. On one hand, an i-
ASF an ibodies may in e e e wi h disease de elopmen , as seen by educed mo ali y, educed
i ulence and a delayed onse o in ec ion in pigs ea ed wi h hose an ibodies (Onisk e al.,
1994; Wa dley e al., 1985). Howe e , con e sely o wha occu s in many di e en animal i al
in ec ions, an ibodies do no neu alise he pa hogenic capaci y o ASFV so ha accines ha
s imula e he de elopmen o he hos humo al immune esponses a e no e icien . On he
o he hand, cellula immune mechanisms as ASF-speci ic cy o oxic T (clus e o di e en ia ion)
CD8+ lymphocy e and na u al kille (NK) cell ac i i ies we e shown o occu in pigs su i ing
expe imen al in ec ion wi h low i ulen NHV isola e (Lei ão e al., 2001; Ma ins e al., 1988,
1993). The cy o oxic T CD8+ lymphocy e ac i i y was seen o play an impo an ole in ASF
p o ec i e immuni y in animals exposed o he low i ulen OUR/T88/3 s ain ha we e no
longe p o ec ed om challenge wi h he i ulen OUR/T88/1 isola e when deple ed o CD8
+
lymphocy es (Ou a e al., 2005). The abo e men ioned immune esponses sugges ha ASFV
speci ic an ibody alone is no su icien o p o ec ion agains ASFV in ec ion, and ha he e is
an impo an ole o he CD8+ lymphocy e subse in ASFV p o ec i e immuni y (Takama su e
al., 2013).
1.2 Whe e ASF-STOP s ands
Soon a e ASF eme ged in Geo gia in 2007 and ca e ully ollowing he de elopmen o he
si ua ion in Russia, he in e na ional scien i ic communi y became awa e o no only he
app oaching h ea o he Eu opean pig indus y bu also he inc eased impo ance o wild boa
in his epidemic. Wi h he aim o unde s and he ole o wild boa in ASF epidemiology, imp o e
diagnosis and su eillance in his species and de elop managemen p ac ices ha would dec ease
he ole o wild boa in ASF epidemiology, a ne wo k o wildli e scien is s, unde he umb ella
o he Eu opean Wildli e Disease Associa ion (EWDA), came oge he o ackle he challenge
o ASF expansion in o new e i o ies. A co e g oup me a a wo kshop in Uppsala, Sweden, on
6-7 Ma ch 2014 o plan a p oposal o he Eu opean Coope a ion in Science and Technology
(COST), a unding o ganisa ion unde he Ho izon 2020 p og amme o he Eu opean Union.
The COST Ac ion (Ac ion is he e m used by COST and i means ‘ne wo king p ojec ’) ASF-
STOP was launched on 1 May 2016. The main objec i e o he Ac ion was ‘ o s op A ican swine
e e om sp eading u he in Eu ope and p o ec ing he Eu opean pig indus y by comba ing
ASF h ough a comp ehensi e, mul i- and in e disciplina y app oach’. The ne wo k included a
b oad a ie y o ields comp ising, among o he s, i ology, wild boa managemen , pa hology,
biosecu i y, accinology and communica ion (Figu e 1.1). The inclusi eness o he ne wo k led
o he in ol emen o esea ch ins i u ions like uni e si ies and e e ina y ins i u es side by side
wi h animal heal h and ood sa e y au ho i ies, hun e s’ associa ions, wildli e manage s and ood
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1. ASF, he pig heal h challenge o he cen u y
Unde s anding and comba ing A ican swine e e 17
and li es ock indus ies. Non-Eu opean pa ne s also joined he ne wo k, sha ed hei expe ience
( om wo k in A ican and p e iously ASF in ec ed coun ies) and con ibu ed o he exchange
o knowledge. Mos Eu opean ins i u ions conduc ing esea ch on ASF pa icipa ed in ASF-
STOP, as well as many ASF na ional and in e na ional e e ence labo a o ies. O e all, he ne wo k
included 37 coun ies; 17 o hem we e inclusi eness a ge coun ies in Eu ope, and h ee
in e na ional Agencies, wi h a o al o almos 300 pa icipan s (Figu e 1.2). All wo ked oge he
in a coo dina ed and in eg a ed e o o collec i ely add ess he mul iple challenges posed by
ASF, mo ing owa ds he common goal o inc easing p epa edness and a emp ing o s op i s
sp ead. ASF-STOP wo ked in close collabo a ion wi h he Global A ican Swine Fe e Resea ch
Alliance (GARA) and pa icipa ed in he c ea ion o a global esea ch agenda (GARA h ps://
www.a s.usda.go /GARA/). In collabo a ion wi h GARA, o acili a e he low o in o ma ion
and, a he same ime, a oid unnecessa y o e lap o duplica ion o e o s, ASF-STOP c ea ed
an inclusi e en i onmen whe e expe s om di e en ields came oge he o complemen each
o he ’s knowledge and build solu ions.
The ne wo k wo ked oge he on coo dina ed objec i es, which included all aspec s connec ed o
ASF (summa ised in his book). High scien i ic excellence, ac i e collabo a ion and in eg a ion o
disciplines led o he achie emen o he objec i es. Special ocus a eas we e he de elopmen o
s anda dised me hods, he iden i ica ion o bes p ac ices applicable o di e en ield condi ions
and he de elopmen o p e en i e measu es, including ad ancing in accine de elopmen .
Mul idisciplina y eams wo ked in close collabo a ion o unde s and he ole o wild boa in
Figu e 1.1. S uc u e o ASF-STOP and o e iew o he main ou pu s.
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C. Ma ins e al.
18 Unde s anding and comba ing A ican swine e e
i us ansmission in di e en condi ions and managemen p ac ices. The eams designed con ol
measu es adap ed o he di e en Eu opean habi a s and wild boa densi ies. Leade s in i ology,
accinology, pa hology, diagnos ics and immunology came oge he o add ess aspec s o he
i us biology, i s e ec s on he hos , po en ial he apies and he bes ways o de ec in ec ion
in animals wi h a ying le els o immunological s a us as well as in samples wi h di e en
p ese a ion condi ions. This la e aspec is pa icula ly ele an in he cu en epidemiological
con ex whe e wild boa , as p o en by he wo k o epidemiologis s and wildli e biologis s in he
ne wo k, cons i u e a new epidemiological cycle o he i us in Eu ope and passi e moni o ing
o wild boa ca casses has p o en c ucial o ea ly de ec ion o ou b eaks. Close moni o ing o
he heal h s a us o wild boa is impo an o he p e en ion o in oduc ion o ASFV in o he
pig p oduc ion sys em. The pig indus y and ood p oduc ion sys em a e ex emely a iega ed in
e ms o size, p ac ices, needs and cul u al impo ance. To p o ec his economically impo an
sec o and he wel a e o he animals, expe s in biosecu i y, pig p oduc ion sys ems and cleaning
and disin ec ion collabo a ed wi h he pig and ood indus y and animal heal h and ood sa e y
au ho i ies o iden i y po en ial isks o ASFV in oduc ion and de ine guidelines speci ic o
di e en b anches o pig p oduc ion, om indus ial o backya d.
ASF-STOP also wo ked owa ds he ollowing capaci y building objec i es: (1) c ea ion o a
Eu ope-wide scien i ic knowledge and echnology exchange pla o m o p e en , con ol and
mi iga e ASF; (2) enabling in o med decision-making based on cu en scien i ic da a; (3)
building capaci y in Eu ope and s eng hening ans-na ional collabo a ion; (4) achie ing
inclusi e collabo a ion; (5) achie ing wide dissemina ion o he ou comes and esul s o ASF-
STOP; and (6) es ablishing a Pan-Eu opean esea ch agenda.
Figu e 1.2. Map o he ASF-STOP pa icipa ing coun ies.
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1. ASF, he pig heal h challenge o he cen u y
Unde s anding and comba ing A ican swine e e 19
Wi hou he collec i e and in eg a ed wo k o ASF-STOP he impac o all hese e o s in
esea ch and de elopmen would ha e been mos ly con ined o speci ic ields. The con inuous
commi men o sha e his in o ma ion wi hin and beyond he ne wo k, communica ing and
engaging policy make s, b eede s and a me s, hun e s, wildli e manage s and socie y as a whole
la gely con ibu ed o he implemen a ion o he knowledge and he impac o ASF-STOP. As a
whole, ASF-STOP made impo an con ibu ions owa ds he con ol and e adica ion o ASF in
Eu ope, de eloped and communica ed new knowledge, buil an ex ended in e na ional ne wo k
o scien is s wo king on ASF and con ibu ed o capaci y building in Eu ope.
1.3 Wha ASF-STOP pa ed he way o
Wi hin he ou yea s o i s li e span, ASF-STOP has aced many challenges and esul ed in e en
mo e success s o ies. A lo has been lea n bu se e al gaps o knowledge ha e been iden i ied
in he p ocess. This book aims o p esen he o e iew o he cu en ly a ailable knowledge on
ASF, wi h special ocus on he Eu opean si ua ion, including bu no limi ed o he esul s o he
Ac ion. This book is also a call o ac ion o he scien i ic communi y o in es iga e hose a eas
ha s ill need o be explo ed, o policy make s and unding bodies o suppo hose e o s and
o socie y o ac i ely engage in he global challenge o s opping ASF.
Recen esea ch on ASFV (Chap e 2) has shown how he i us inhibi s di e en immune
esponses and how mul iple ac o s can lead o di e en le hali y a es and ha , al hough
knowledge on he a chi ec u e o ASFV has p og essed o e ime, mo e ligh needs o be shed on
his aspec . A he same ime, Chap e 2 shows how genome and compu a ional me hods could
p o e undamen al o he de elopmen o an i i al d ugs and a accine.
The immune sys em is an o ganism ba ie agains ha m ul pa hogens and while he hos
immune sys em eac s o ASFV in ec ion, he i us in e ac ions wi h mac ophages o dend i ic
cells emain la gely unknown, as is he immune esponse o ASFV in na u al in ec ions compa ed
o expe imen al se ings (Chap e 3).
Knowledge on pa hology p o ides he ounda ion o unde s anding pa hogenesis and hos
esponse o he pa hogen. Disease caused by ASFV may ange om pe acu e o subclinical
o inappa en depending on di e en ac o s, among which he i ulence o he isola es is
pa icula ly impo an . The p esence and se e i y o lesions a e highly a iable and may a ec
mul iple o gans (Chap e 4).
Building on his body o knowledge on he lesions caused by ASF, he immunological p ocesses
and he cha ac e is ics o he i us se e al diagnos ic ools ha e been de eloped wi h good
sensi i i y and speci ici y (Chap e 5). Howe e , i emains o pa amoun impo ance o ca e ully
ollow guidelines o he choice o he mos app op ia e ool and sampling p ocedu e based on
he si ua ion a hand, he ield condi ions and he equi emen s.
An aspec ha has gained enewed a en ion o e he pas ew decades is he de elopmen o
a accine. O e ime mul iple app oaches ha e been es ed bu mos o hem we e ei he no
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