MeaslesIn developedcountriesmeasles

Measles
In developedcountriesmeaslesisconsideredatrivialdiseaseof
childhood butindevelopingcountriesintheabsenceofvaccina-
tion thedeathratecanbeashighas30%;thesituationin19th
century Londonwassimilar.Intheabsenceofglobalvaccination
programmesitisestimatedthat6millionchildrenwoulddieof
measles peryear,mostlyofpneumonia,otherrespiratorycompli-
cations ordiarrohea.Thevaccinesdevelopedinthe1960sto1980s
arethereforelifesavingadditionstoimmunisationprogrammes.
Measles isacomplicateddiseaseandanormalinfectionwith
recoverywithinweekscausesprolongedimmunedisruptionover
a periodofayearormore,whichforexampleaffectstheresponse
to tuberculosisandsomeimmunemediatedsyndromes(Moss
et al.,2004). Killedmeaslesvaccinesweredevelopedinthe1960s
using aprocessinvolvingformalintreatmentsimilartothatused
for themanufactureofinactivatedpoliovaccines;someatleast
involvedaluminiumhydroxideadjuvantswhichmayhavebeena
factor inwhatfollowed.Theprotectiontheygavedeclinedinthe
medium tolongtermandwhenimmunisedindividualswerethen
exposedtowildtypemeaslestheydevelopedaseriousdisease
with anatypicalrashandahighrateoflunginvolvementwhich
could requirehospitalisation(Fulginiti etal.,1967). Nodeathswere
recorded.Thesusceptibilitytoatypicalmeaslespersistedformany
years;onecasewasreported15yearsafterimmunisation
(Fulginiti andHeller,1980). Initiallytheaberrantresponsewas
attributed tothe finding thattheformalintreatmenthad
destroyedtheimmunogenicpropertiesofthefusionprotein
(Norrbyetal.,1975). Theconsequentabsenceofantibodiesmeant
that whilecellfreeviruswouldbeneutralisedtheviruscould
avoidneutralisingantibodiesbyspreadingfromcelltocellbycell
fusion. Laterstudiesinnon-humanprimatemodelsconcludedthat
the syndromeresultedfromprimingforaninappropriatenon-
protectivetype2CD4T-cellresponsewhichmeantthatnon-
protectivebutbiologicallyactiveantiFproteinantibodieswere
induced morerapidlythaninnaïveanimals;therewasnolackof
antibodies againsttheFprotein(Polack etal.,1999). Atypical
measles raisesissuesofthesuitabilityofsometypesofkilled
vaccineseventoday.Similarmoreseriousreactionswerealso
recordedwithvaccinesagainstRespiratorySyncitialvirus,another
paramyxovirus,wheredeathsoccurred(Kim etal.,1968). However
despite thesubtletiesoftheimmuneresponsetheserological
responsetomeaslesasmeasuredbyneutralisingantibodyis
acceptedasthebestmarkerofprotectionfrominfection.Protec-
tivelevelshavebeendefined (Chen etal.,1990).
Wild typemeaslescausesfatal acuteencephalitisinsome
instances.Itcanalsocausesubacutesclerosingpanencephalitis
(SSPE)upto10yearsaftertheoriginalinfection,asaresultofchronic
viruspersistenceinthebrainofvictims.VariousgenesofSSPEstrains
particularlythefusiongenearedeletedormodified (Schmidetal.,
1992).TheroleoflivemeaslesinSSPEwasnotdiscovereduntilafter
thedevelopmentoftheliveattenuatedvaccinesandmighthave
causedconcernovervaccineuse.Thevaccineshaveinfactprevented
manydeathsandhaveneverbeenimplicatedinSSPE.Measles
vaccineshoweverareclearlyapotentialminefield.
The first isolationofmeaslesviruswasdescribedin1954(Enders
and Peebles,1954) andthevirusisnamedtheEdmonstonstrainafter
the childconcerned.Isolationusedprimaryhumankidneyand
primaryhumanamnioncellsandtheviruswassubsequently
passaged12timesinembryonatedchickeneggsand19timesin
primarychickembryo fibroblasttoproducethe first candidate
measlesvaccine.TheEdmonstonBvaccinewasderivedfromthis
strainbyafurther five passagesinchickembryo fibroblastsat36–
37 1C.Itwasassociatedwithfeverandwasinitiallygivenwith
immunoglobulintoreduceitsvirulencefurther;productionlotsin
cell cultureweresaidtobelessreactogenicandwerelicensedforuse
withorwithoutimmunoglobulin.Otherstrainsweredevelopedfrom
the Edmonstonstrain,andanoutlineofsomeoftheresulting
vaccinesstillinglobaluseisgivenin Fig. 4. Inlateryearstherewere
attemptstodevelopaconvincinganimalmodelanditwasshown
that theisolationofthevirusintheusualcelltypessuchasVeroor
humandiploidcellsgaverisetoavirusthatwouldnotcausemeasles
inprimatestothesamedegreeasunpassagedvirus(Kobuneetal.,
1996;vanBinnendijketal.,1994). Isolationinperipheralblood
lymphocytesorthemarmosetBcelllineB95agavevirusesthat
werevirulent,andalsoimprovedtheisolationrate,suggestingthat
thevirusesaremorelikethewildtype,andcellsinfectedindisease
aresimilartothelymphocytelines(Kobuneetal.,1990).
The MoratenstrainwasderivedfromEdmonstonBby40further
passagesinchickcellcultureat321 (Hillemanetal.,1968); the
Schwarzstrainby85furtherpassagesofEdmonstonAinchickcells
(Schwarz,1962) andEdmonstonZagrebbypassageofEdmonstonBin
the humandiploid fibroblastlineWI38(Ikicetal.,1970,1972). The
AIK-CstrainwasderivedfromtheoriginalEdmonstonBbygrowthat
lowtemperatureinchickcells(Hirayama,1983;Makino,1983)

Results (Indonesian) 1:

CampakDi developedcountriesmeaslesisconsideredatrivialdiseaseofmasa kanak-kanak butindevelopingcountriesintheabsenceofvaccina-tion thedeathratecanbeashighas30%; thesituationin19thabad ke Londonwassimilar.Intheabsenceofglobalvaccinationprogrammesitisestimatedthat6millionchildrenwoulddieofcampak peryear, mostlyofpneumonia, otherrespiratorycompli-kation ordiarrohea. Thevaccinesdevelopedinthe1960sto1980sarethereforelifesavingadditionstoimmunisationprogrammes.Isacomplicateddiseaseandanormalinfectionwith campakrecoverywithinweekscausesprolongedimmunedisruptionoverperiodofayearormore, whichforexampleaffectstheresponseuntuk tuberculosisandsomeimmunemediatedsyndromes (Mosset al., 2004). Killedmeaslesvaccinesweredevelopedinthe1960smenggunakan aprocessinvolvingformalintreatmentsimilartothatuseduntuk themanufactureofinactivatedpoliovaccines; someatleastinvolvedaluminiumhydroxideadjuvantswhichmayhavebeenafaktor inwhatfollowed. Theprotectiontheygavedeclinedinthetolongtermandwhenimmunisedindividualswerethen menengahexposedtowildtypemeaslestheydevelopedaseriousdiseasedengan anatypicalrashandahighrateoflunginvolvementwhichbisa requirehospitalisation (Fulginiti etal., 1967). Nodeathsweredirekam. Thesusceptibilitytoatypicalmeaslespersistedformanytahun; onecasewasreported15yearsafterimmunisation(Fulginiti andHeller, 1980). Initiallytheaberrantresponsewasdikaitkan dengan thattheformalintreatmenthad menemukandestroyedtheimmunogenicpropertiesofthefusionprotein(Norrbyetal., 1975). Theconsequentabsenceofantibodiesmeantwhilecellfreeviruswouldbeneutralisedtheviruscould ituavoidneutralisingantibodiesbyspreadingfromcelltocellbycellfusi. Laterstudiesinnon-humanprimatemodelsconcludedthatsyndromeresultedfromprimingforaninappropriatenon-protectivetype2CD4T-cellresponsewhichmeantthatnon -protectivebutbiologicallyactiveantiFproteinantibodieswerediinduksi morerapidlythaninnaïveanimals; therewasnolackofantibodi againsttheFprotein (Polack etal., 1999). Atipikalraisesissuesofthesuitabilityofsometypesofkilled campakvaccineseventoday. SimilarmoreseriousreactionswerealsorecordedwithvaccinesagainstRespiratorySyncitialvirus, lainparamyxovirus, wheredeathsoccurred (Kim etal., 1968). NamunMeskipun thesubtletiesoftheimmuneresponsetheserologicalresponsetomeaslesasmeasuredbyneutralisingantibodyisacceptedasthebestmarkerofprotectionfrominfection. ProTec-tivelevelshavebeendefined (Chen etal., 1990).Liar typemeaslescausesfatal acuteencephalitisinsomecontoh. ItcanalsocausesubacutesclerosingpanencephalitisUpto10yearsaftertheoriginalinfection (SSPE), asaresultofchronicviruspersistenceinthebrainofvictims. VariousgenesofSSPEstrainsparticularlythefusiongenearedeletedormodified (Schmidetal.,1992). TheroleoflivemeaslesinSSPEwasnotdiscovereduntilafterthedevelopmentoftheliveattenuatedvaccinesandmighthavecausedconcernovervaccineuse. ThevaccineshaveinfactpreventedmanydeathsandhaveneverbeenimplicatedinSSPE.Measlesvaccineshoweverareclearlyapotentialminefield.Isolationofmeaslesviruswasdescribedin1954 pertama (selesaidan Peebles, 1954) andthevirusisnamedtheEdmonstonstrainafterchildconcerned. Isolationusedprimaryhumankidneyandprimaryhumanamnioncellsandtheviruswassubsequentlypassaged12timesinembryonatedchickeneggsand19timesinprimarychickembryo fibroblasttoproducethe pertama calonmeaslesvaccine. TheEdmonstonBvaccinewasderivedfromthisstrainbyafurther lima passagesinchickembryo fibroblastsat36-37 1C. Itwasassociatedwithfeverandwasinitiallygivenwithimmunoglobulintoreduceitsvirulencefurther; productionlotsinsel cultureweresaidtobelessreactogenicandwerelicensedforusewithorwithoutimmunoglobulin. OtherstrainsweredevelopedfromEdmonstonstrain, andanoutlineofsomeoftheresultingvaccinesstillinglobaluseisgivenin gambar 4. InlateryearstherewereattemptstodevelopaconvincinganimalmodelanditwasshowntheisolationofthevirusintheusualcelltypessuchasVeroor ituhumandiploidcellsgaverisetoavirusthatwouldnotcausemeaslesinprimatestothesamedegreeasunpassagedvirus(Kobuneetal.,1996; vanBinnendijketal., 1994). IsolationinperipheralbloodlymphocytesorthemarmosetBcelllineB95agavevirusesthatwerevirulent, andalsoimprovedtheisolationrate, suggestingthatthevirusesaremorelikethewildtype, andcellsinfectedindiseasearesimilartothelymphocytelines(Kobuneetal.,1990).MoratenstrainwasderivedfromEdmonstonBby40furtherpassagesinchickcellcultureat321 (Hillemanetal., 1968); TheSchwarzstrainby85furtherpassagesofEdmonstonAinchickcells(Schwarz, 1962) andEdmonstonZagrebbypassageofEdmonstonBinhumandiploid fibroblastlineWI38(Ikicetal.,1970,1972). TheAIK-CstrainwasderivedfromtheoriginalEdmonstonBbygrowthatlowtemperatureinchickcells (Hirayama, 1983; Makino, 1983)

Results (Indonesian) 2:

Campak
Di developedcountriesmeaslesisconsideredatrivialdiseaseof
masa butindevelopingcountriesintheabsenceofvaccina-
tion thedeathratecanbeashighas30%; thesituationin19th
abad Londonwassimilar.Intheabsenceofglobalvaccination
programmesitisestimatedthat6millionchildrenwoulddieof
campak pertahun, mostlyofpneumonia, otherrespiratorycompli-
kation ordiarrohea.Thevaccinesdevelopedinthe1960sto1980s
. Arethereforelifesavingadditionstoimmunisationprogrammes
campak isacomplicateddiseaseandanormalinfectionwith
recoverywithinweekscausesprolongedimmunedisruptionover
sebuah periodofayearormore, whichforexampleaffectstheresponse
(Moss untuk tuberculosisandsomeimmunemediatedsyndromes
. Et al, 2004). Killedmeaslesvaccinesweredevelopedinthe1960s
menggunakan aprocessinvolvingformalintreatmentsimilartothatused
untuk themanufactureofinactivatedpoliovaccines; someatleast
involvedaluminiumhydroxideadjuvantswhichmayhavebeena
faktor inwhatfollowed.Theprotectiontheygavedeclinedinthe
menengah tolongtermandwhenimmunisedindividualswerethen
exposedtowildtypemeaslestheydevelopedaseriousdisease
dengan anatypicalrashandahighrateoflunginvolvementwhich
bisa requirehospitalisation (Fulginiti dkk, 1967.). Nodeathswere
recorded.Thesusceptibilitytoatypicalmeaslespersistedformany
tahun; onecasewasreported15yearsafterimmunisation
(Fulginiti andHeller, 1980). Initiallytheaberrantresponsewas
dikaitkan tertalu menemukan thattheformalintreatmenthad
destroyedtheimmunogenicpropertiesofthefusionprotein
(Norrbyetal., 1975). Theconsequentabsenceofantibodiesmeant
yang whilecellfreeviruswouldbeneutralisedtheviruscould
avoidneutralisingantibodiesbyspreadingfromcelltocellbycell
fusion. Laterstudiesinnon-humanprimatemodelsconcludedthat
yang syndromeresultedfromprimingforaninappropriatenon-
protectivetype2CD4T-cellresponsewhichmeantthatnon-
protectivebutbiologicallyactiveantiFproteinantibodieswere
diinduksi morerapidlythaninnaïveanimals; therewasnolackof
(. Polack dkk, 1999) antibodi againsttheFprotein. Atypical
campak raisesissuesofthesuitabilityofsometypesofkilled
vaccineseventoday.Similarmoreseriousreactionswerealso
recordedwithvaccinesagainstRespiratorySyncitialvirus, lain
paramyxovirus, wheredeathsoccurred (Kim et al., 1968). Namun
meskipun thesubtletiesoftheimmuneresponsetheserological
responsetomeaslesasmeasuredbyneutralisingantibodyis
acceptedasthebestmarkerofprotectionfrominfection.Protec-
tivelevelshavebeendefined (Chen dkk., 1990).
Typemeaslescausesfatal liar acuteencephalitisinsome
instances.Itcanalsocausesubacutesclerosingpanencephalitis
(SSPE) upto10yearsaftertheoriginalinfection, asaresultofchronic
viruspersistenceinthebrainofvictims.VariousgenesofSSPEstrains
particularlythefusiongenearedeletedormodified (Schmidetal.,
1992) .TheroleoflivemeaslesinSSPEwasnotdiscovereduntilafter
thedevelopmentoftheliveattenuatedvaccinesandmighthave
causedconcernovervaccineuse.Thevaccineshaveinfactprevented
manydeathsandhaveneverbeenimplicatedinSSPE.Measles
vaccineshoweverareclearlyapotentialminefield.
The isolationofmeaslesviruswasdescribedin1954 pertama (Enders
dan Peebles, 1954) andthevirusisnamedtheEdmonstonstrainafter
yang childconcerned.Isolationusedprimaryhumankidneyand
primaryhumanamnioncellsandtheviruswassubsequently
passaged12timesinembryonatedchickeneggsand19timesin
primarychickembryo fibroblasttoproducethe kandidat pertama
measlesvaccine.TheEdmonstonBvaccinewasderivedfromthis
strainbyafurther lima passagesinchickembryo fibroblastsat36-
37 1C.Itwasassociatedwithfeverandwasinitiallygivenwith
immunoglobulintoreduceitsvirulencefurther; productionlotsin
sel cultureweresaidtobelessreactogenicandwerelicensedforuse
withorwithoutimmunoglobulin.Otherstrainsweredevelopedfrom
yang Edmonstonstrain, andanoutlineofsomeoftheresulting
vaccinesstillinglobaluseisgivenin Gambar. 4. Inlateryearstherewere
attemptstodevelopaconvincinganimalmodelanditwasshown
yang theisolationofthevirusintheusualcelltypessuchasVeroor
humandiploidcellsgaverisetoavirusthatwouldnotcausemeasles
inprimatestothesamedegreeasunpassagedvirus (Kobuneetal,.
1996;. VanBinnendijketal, 1994). Isolationinperipheralblood
lymphocytesorthemarmosetBcelllineB95agavevirusesthat
werevirulent, andalsoimprovedtheisolationrate, suggestingthat
thevirusesaremorelikethewildtype, andcellsinfectedindisease
aresimilartothelymphocytelines (Kobuneetal, 1990.).
The MoratenstrainwasderivedfromEdmonstonBby40further
passagesinchickcellcultureat321 (Hillemanetal 1968.); yang
Schwarzstrainby85furtherpassagesofEdmonstonAinchickcells
(Schwarz, 1962) andEdmonstonZagrebbypassageofEdmonstonBin
yang fibroblastlineWI38 humandiploid (Ikicetal., 1970,1972). The
AIK-CstrainwasderivedfromtheoriginalEdmonstonBbygrowthat
lowtemperatureinchickcells (Hirayama, 1983; Makino, 1983)