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 encephalitis in some
instances.It can also cause subacute sclerosing pan encephalitis
(SSPE)up to 10 years after the original infection,as are sultofchronic
virus persistence in the brain of victims.Various genes of SSPE strains
particularly the fusion gene are deleted or modified (Schmidetal.,
1992).The roleof live measles in SSPE was not discovered until after
the development of the live attenuated vaccines and might have
caused concern over vaccineuse.Thev accines have in fact prevented
many deaths and have never been implicatedinS SPE.Measles
vaccines how everare clearly apotential minefield.
The first isolation of measles virus was described in 1954(Enders
and Peebles,1954) and the virus is named the Edmonston strain after
the child concerned.Isolation used primary human kidney and
primary human amnion cells and the virus was subsequently
passaged 12 times in embryonted chicken eggs and 19 times in
primary chick embryo fibroblast to produce the first candidate
measle svaccine. The Edmonston B vaccine was derived from this
strain by a further five passages in chick embryo fibroblasts at36–
37 1C.It was associated with fever and was initially given with
immunoglobulin to reduce its virulence further;production lots in
cell culture were said to be less reactogenic and were licensed for use
with or without immunoglobulin. Other strains were developed from
the Edmonston strain,and an outline of some of there sulting
vaccines still in global use is given in Fig. 4. In later years there were
attempts to develop a convincing animal model and it was shown
that the isolation of the virus in the usual cell types such as Vero or
human diploid cells gave rise to a virus that would not cause measles
in primates to the same degree as unpassaged virus(Kobuneetal.,
1996;vanBinnendijketal.,1994).

Results (Indonesian) 1:

CampakNegara-negara maju campak dianggap sepele penyakitkecil tapi indeveloping negara tanpa adanya vaccina-tion angka kematian dapat setinggi 30%; situasi di 19abad ke London adalah serupa. Dalam ketiadaan global vaksinasiprogram-program yang diperkirakan bahwa 6 juta anak-anak akan maticampak per tahun, sebagian besar dari pneumonia, kelas pernapasan lain-kation atau diarrohea. Vaksin yang dikembangkan pada 1960-an untuk tahun 1980oleh karena itu hidup menyimpan tambahan untuk program-program imunisasi. Campak adalah infeksi penyakit dan anormal yang rumit denganpemulihan dalam minggu menyebabkan gangguan kekebalan yang berkepanjangan selamaperiode ayear atau lebih, yang misalnya mempengaruhi responuntuk tuberkulosis dan someimmunemediated sindrom (Mosset al., 2004). Membunuh campak vaksin dikembangkan pada 1960-anmenggunakan aprocess yang melibatkan pengobatan formalin yang mirip dengan yang digunakanuntuk pembuatan inactivated poliovaccines; beberapa setidaknyaterlibat eadjuvants hydroxid aluminium yang mungkin telahfaktor apa yang diikuti. Perlindungan yang mereka berikan menurun dalammenengah dan panjang termand ketika immunis edindividuals kemudianterkena campak jenis liar mereka developeda penyakit seriusdengan ruam atipikal dan tingkat tinggi keterlibatan paru-paru yangbisa memerlukan rawat inap disertai (Fulginiti etal., 1967). Tidak swere kematiandirekam. Kerentanan terhadap campak atipikal Carnegie banyaktahun; salah satu kasus yang dilaporkan 15 tahun sesudah imunisasi(Fulginiti andHeller, 1980). Awalnya tanggapan menyimpang adalahdikaitkan dengan temuan itu pengobatan formalinmenghancurkan sifat immunogenic protein fusi(Norrbyetal., 1975). Akibatnya tidak adanya antibodi dimaksudkanbahwa sementara sel virus gratis akan menetralisir virus bisamenghindari peneutralan antibodi dengan menyebarkan dari sel ke sel oleh selfusi. Kemudian studi dalam model primata non-manusia menyimpulkan bahwaSindrom akibat priming untuk aninappropriate non-pelindung jenis 2CD4T-sel respon yang berarti thatnon-pelindung tapi biologis aktif anti Fprotein antibodi yangdiinduksi lebih cepat daripada innaïveanimals; ada kekurangan tidak adaantibodi terhadap Fprotein (Polack etal., 1999). Atipikalcampak menimbulkan isu-isu tentang kesesuaian sometypes dari membunuhvaksin bahkan hari ini. Reaksi serupa yang lebih serius yang jugadirekam dengan vaksin terhadap pernapasan Syncitialvirus, lainparamyxovirus, wheredeathsoccurred (Kim etal., 1968). NamunMeskipun seluk-beluk respon imun serologicalRespon untuk campak yang diukur dengan antibodi peneutralanditerima sebagai penanda terbaik perlindungan dari infeksi. ProTec-tive tingkat telah didefinisikan (Chen etal., 1990).Jenis liar campak menyebabkan ensefalitis akut fatal dalam beberapacontoh. Juga dapat menyebabkan sclerosing subakut pan ensefalitis(SSPE) hingga 10 tahun setelah infeksi asli, karena sultofchronicvirus ketekunan dalam otak korban. Berbagai gen SSPE galurterutama fusi gen yang dihapus atau diubah (Schmidetal.,1992). Campak hidup roleof SSPE tidak ditemukan sampai setelahpengembangan hidup dilemahkan vaksin dan mungkin memilikimenimbulkan kekhawatiran atas vaccineuse. Thev accines bahkan mencegahbanyak kematian dan tidak pernah implicatedinS SPE. Campakvaksin bagaimana everare jelas apotential ladang ranjau.Isolasi pertama virus campak digambarkan pada tahun 1954 (selesaidan Peebles, 1954) dan virus bernama Edmonston ketegangan setelahanak yang bersangkutan. Isolasi digunakan utama ginjal manusia dansel-sel amnion manusia utama dan virus menjabatpassaged 12 kali dalam embryonted telur ayam dan 19 kalicewek utama embrio fibroblast menghasilkan calon pertamameasle svaccine. Vaksin Edmonston B berasal dari iniketegangan dengan lebih lanjut lima bagian cewek embrio fibroblas at36-37 1C. Itu dikaitkan dengan demam dan awalnya diberikan denganbanyak produksi antibodi untuk mengurangi virulensi yang lebih lanjut;kultur sel dikatakan kurang reactogenic dan yang berlisensi untuk penggunaandengan atau tanpa antibodi. Strain lain dikembangkan dariketegangan Edmonston, dan garis besar dari beberapa ada sultingvaksin masih dalam penggunaan global diberikan dalam gambar 4. Di tahun-tahun berikutnya yang adaupaya untuk mengembangkan model hewan yang meyakinkan dan itu ditunjukkanisolasi virus pada sel biasa jenis seperti Vero atausel-sel manusia diploid memunculkan virus yang tidak akan menyebabkan campakpada primata derajat yang sama sebagai unpassaged virus(Kobuneetal.,1996; vanBinnendijketal., 1994).