MeaslesIn developed countries measl

Measles
In developed countries measles is considered a trivial disease of
childhood but indeveloping countries in the absence of vaccina-
tion the death rate can be as high as 30%; the situation in 19th
century London was similar.In the absence of global vaccination
programmes it is estimated that 6 million children would die of
measles per year,mostly of pneumonia,other respiratory compli-
cations or diarrohea. The vaccines developed in the 1960s to 1980s
are therefore life saving additions to immunisation programmes.
Measles is a complicated disease and anormal infection with
recovery within weeks causes prolonged immune disruption over
a period of ayear or more,which for example affects the response
to tuberculosis and someimmunemediated syndromes(Moss
et al.,2004). Killed measles vaccines were developed in the 1960s
using aprocess involving formalin treatment similar to that used
for the manufacture of inactivated poliovaccines;some at least
involved aluminium hydroxid eadjuvants which may have been a
factor in what followed. The protection they gave declined in the
medium to long termand when immunis edindividuals were then
exposed to wild type measles they developeda serious disease
with an atypical rash and a high rate of lung involvement which
could require hospitalisation (Fulginiti etal.,1967). No death swere
recorded.The susceptibility to atypical measles persisted for many
years; one case was reported 15 years after immunisation
(Fulginiti andHeller,1980). Initially the aberrant response was
attributed to the finding that the formalin treatment had
destroyed the immunogenic properties of the fusion protein
(Norrbyetal.,1975). The consequent absence of antibodies meant
that while cell free virus would be neutralised the virus could
avoid neutralising antibodies by spreading from cell to cell by cell
fusion. Later studies in non-human primate models concluded that
the syndrome resulted from priming for aninappropriate non-
protective type 2CD4T-cell response which meant thatnon-
protective but biologically active anti Fprotein antibodies were
induced more rapidly than innaïveanimals;there was no lack of
antibodies against the Fprotein(Polack etal.,1999). Atypical
measles raises issues of the suitability of sometypes of killed
vaccines even today. Similar more serious reactions were also
recorded with vaccines against Respiratory Syncitialvirus, another
paramyxovirus,wheredeathsoccurred(Kim etal.,1968). However
despite the subtleties of the immune response the serological
response to measles as measured by neutralising antibody is
accepted as the best marker of protection from infection.Protec-
tive levels have been defined (Chen etal.,1990).
Wild type measles causes fatal acute encephaliti sinsome
instances.It can also causesubacutesclerosingpanencephalitis
(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:

MeaslesIn developed countries measles is considered a trivial disease ofchildhood but indeveloping countries in the absence of vaccina-tion the death rate can be as high as 30%; the situation in 19thcentury London was similar.In the absence of global vaccinationprogrammes it is estimated that 6 million children would die ofmeasles per year,mostly of pneumonia,other respiratory compli-cations or diarrohea. The vaccines developed in the 1960s to 1980sare therefore life saving additions to immunisation programmes. Measles is a complicated disease and anormal infection withrecovery within weeks causes prolonged immune disruption overa period of ayear or more,which for example affects the responseto tuberculosis and someimmunemediated syndromes(Mosset al.,2004). Killed measles vaccines were developed in the 1960susing aprocess involving formalin treatment similar to that usedfor the manufacture of inactivated poliovaccines;some at leastinvolved aluminium hydroxid eadjuvants which may have been afactor in what followed. The protection they gave declined in themedium to long termand when immunis edindividuals were thenexposed to wild type measles they developeda serious diseasewith an atypical rash and a high rate of lung involvement whichcould require hospitalisation (Fulginiti etal.,1967). No death swererecorded.The susceptibility to atypical measles persisted for manyyears; one case was reported 15 years after immunisation(Fulginiti andHeller,1980). Initially the aberrant response wasattributed to the finding that the formalin treatment haddestroyed the immunogenic properties of the fusion protein(Norrbyetal.,1975). The consequent absence of antibodies meantthat while cell free virus would be neutralised the virus couldavoid neutralising antibodies by spreading from cell to cell by cellfusion. Later studies in non-human primate models concluded thatthe syndrome resulted from priming for aninappropriate non-protective type 2CD4T-cell response which meant thatnon-protective but biologically active anti Fprotein antibodies wereinduced more rapidly than innaïveanimals;there was no lack ofantibodies against the Fprotein(Polack etal.,1999). Atypicalmeasles raises issues of the suitability of sometypes of killedvaccines even today. Similar more serious reactions were alsorecorded with vaccines against Respiratory Syncitialvirus, anotherparamyxovirus,wheredeathsoccurred(Kim etal.,1968). Howeverdespite the subtleties of the immune response the serologicalresponse to measles as measured by neutralising antibody isaccepted as the best marker of protection from infection.Protec-tive levels have been defined (Chen etal.,1990).Wild type measles causes fatal acute encephaliti sinsomeinstances.It can also causesubacutesclerosingpanencephalitis(SSPE)upto10yearsaftertheoriginalinfection,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).The MoratenstrainwasderivedfromEdmonstonBby40furtherpassagesinchickcellcultureat321 (Hillemanetal.,1968); theSchwarzstrainby85furtherpassagesofEdmonstonAinchickcells(Schwarz,1962) andEdmonstonZagrebbypassageofEdmonstonBinthe humandiploid fibroblastlineWI38(Ikicetal.,1970,1972). TheAIK-CstrainwasderivedfromtheoriginalEdmonstonBbygrowthatlowtemperatureinchickcells(Hirayama,1983;Makino,1983)

Results (Indonesian) 2:

Campak
Di negara-negara campak dikembangkan dianggap penyakit sepele
kecil tapi indeveloping negara dengan tidak adanya vaksinasi
tion tingkat kematian bisa setinggi 30%; situasi di 19
abad London similar.In tidak adanya vaksinasi global yang
program diperkirakan 6 juta anak-anak akan meninggal
campak per tahun, sebagian besar pneumonia, komplikasi pernapasan lainnya
kation atau diarrohea. Vaksin yang dikembangkan pada tahun 1960 untuk tahun 1980
karena itu menyimpan penambahan program imunisasi hidup.
Campak adalah penyakit yang rumit dan anormal infeksi
pemulihan dalam beberapa minggu menyebabkan gangguan kekebalan berkepanjangan selama
periode ayear atau lebih, yang misalnya mempengaruhi respon
untuk tuberkulosis dan sindrom someimmunemediated (Moss
et al., 2004). Membunuh vaksin campak dikembangkan pada tahun 1960
menggunakan aprocess melibatkan pengobatan formalin mirip dengan yang digunakan
untuk pembuatan poliovaccines tidak aktif, beberapa setidaknya
terlibat aluminium eadjuvants hydroxid yang mungkin telah menjadi
faktor dalam apa yang diikuti. Perlindungan mereka memberi menurun di
media untuk termand panjang ketika edindividuals immunis kemudian
terkena jenis campak liar mereka developeda penyakit serius
dengan ruam atipikal dan tingkat keterlibatan yang tinggi paru yang
bisa memerlukan rawat inap (Fulginiti dkk., 1967). Tidak ada kematian swere
recorded.The kerentanan terhadap campak atipikal bertahan selama bertahun-
tahun; satu kasus dilaporkan 15 tahun setelah imunisasi
(Fulginiti andHeller, 1980). Awalnya respon yang menyimpang itu
dikaitkan dengan temuan bahwa perlakuan formalin telah
menghancurkan sifat imunogenik dari protein fusi
(Norrbyetal., 1975). Tidak adanya konsekuen antibodi berarti
bahwa sementara virus gratis cell akan dinetralisir virus bisa
menghindari antibodi penetralisir dengan menyebarkan dari sel ke sel oleh sel
fusi. Studi di kemudian model primata non-manusia menyimpulkan bahwa
sindrom yang dihasilkan dari priming untuk aninappropriate non
Jenis pelindung respon-sel 2CD4T yang berarti thatnon-
antibodi anti Fprotein pelindung tapi biologis aktif yang
diinduksi lebih cepat dari innaïveanimals; tidak ada kekurangan
antibodi terhadap yang Fprotein (Polack dkk., 1999). Atypical
campak menimbulkan masalah kesesuaian sometypes dari membunuh
vaksin bahkan hari ini. Reaksi yang lebih serius serupa juga
direkam dengan vaksin terhadap pernapasan Syncitialvirus, lain
paramyxovirus, wheredeathsoccurred (Kim et al., 1968). Namun
meskipun seluk-beluk respon kekebalan serologis
menanggapi campak yang diukur dengan antibodi yang
diterima sebagai penanda terbaik perlindungan dari infection.Protec-
tingkat tive telah ditetapkan (Chen dkk., 1990).
Jenis campak liar menyebabkan akut yang fatal encephaliti sinsome
instances.It juga causesubacutesclerosingpanencephalitis
(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)