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1 1918~19.. "..,." 2002,, SARS [1, 2]., ,,.,., , , : 05/3/4 : 05/9/16 : ( ) TEL : 053) FAX : 053) songdy@hitel.net... Fig. 1 A, H, J, B 9. C, D, E, F, G, I K. [3]. 55 (WHO) 3 12,,,,... WHO WHO , 774 [4]. 11%., 65 50%. 1/5 [5]. 3 17, , ,,,

2 [6].,,,. Peiris [7], Drosten [5]. 2003 4 16 WHO, SARS-associated coronavirus(sars-cov).,, RNA. 50 45, [7, 8, 9].

2 2 [6].,,,. Peiris [7], Drosten [5] WHO, SARS-associated coronavirus(sars-cov).,, RNA , [7, 8, 9]. (Torovirus) (Coronaviridae)., 4 1 (HCoV-229E ),,,,, 2 (HCoV-OC43 ),,,,, 3,, 4 (SARS) Fig. 1. Chain of transmission among guests at Hotel M-Hong Kong, 2003

3 107 중증 급성 호흡기 증후군 Fig. 2. The nucleotide-sequence alignment of fragment BNI-1 with known coronaviruses. 며, 단일가닥의 양성극성(positive-sense) RNA 유전자를 가진다(20~30kb, MW 5~6 106). 나선형의 뉴클레오캡시드 단백은 직경이 9~11nm이며 외피에는 태양광환 모양으로 20nm 길이의 곤봉 혹은 꽃잎 모양의 표면 돌기(spike)들 이 존재한다. Fig. 3. A phylogenetic tree shows relations among coronavirus polymerase gene fragments (corresponding to BNI-1) according to the neighbor-joining method. 분리된 사스코로나 바이러스(SARS-CoV)이다. 2003년 4 월에는 사스-코로나바이러스 Tor2 주의 전체 염기서열이 규명(29,736-bps, Genebank accession number AY274119) 되었다(Fig 2, 3). 코로나바이러스는 80~220nm 크기에 외피를 갖고 있으 바이러스 단백으로는 뉴클레오캡시드(50~60kDa), 막 (M) 당단백(20~30 kda), 스파이크(S) 당 단백 ( kda)이 존재한다. 사람 코로나바이러스 OC43주 등 일부 바이러스에서는 혈구응집에 관여하는 세 번째 당단백을 갖고 있다. 코로나바이러스의 유전자는 Pol(RNA 중합효 소)-S(스파이크 당단백)-E(외피단백)-M(막 당단백)-N(뉴 클레오캡시드)의 순서로 배열되어 있다. 코로나바이러스 의 증식은 세포질에서 이루어지지만 세포배양은 어렵다. 첫 번째 단계로 바이러스 표면의 스파이크 당단백이 숙 주세포의 수용체에 결합하는데, 사람 코로나바이러스 229E주의 수용체는 aminopeptidase N이다. 이어서 바이러 스 입자가 세포내 이입(endocytosis)에 의해서 세포내로 이동한 뒤 탈외피(uncoating) 단계를 거친다. 바이러스

4 RNA RNA RNA. 5~6 subgenomic mrna (template) RNA ( ). subgenomic mrna. genomic RNA (RER). (vesicle). (deletion mutation). (recombination) RNA., 1-2 4, 48. 4~80 21.,. SARS-CoV. 4 2, 1 PCR. 6 PCR,. SARS-CoV. coronavirus SARS [10]. 3~ %( 45%). (Basic reproduction number, Ro) Ro=2.7[95% CI:2.2~3.7] [11]., 3. "Super spread" 0~8.5% 60~73%. SARS,, virus [12].,,, 10 ~14 100%, 90%, 40~50% %., , 10.,,....,., ( 2 ).,,. (social contact).. 10., [5]. 38,

5 ,,,. 3~7,,. 80~90% 6~7 10% (acute respiratory distress syndrome). 100%.,, 66%., 20~40%. 20~ 30%. 70~90%,, LDH. 2, 3, 30% 5. LDH, LDH,. 70~80%.,. 1~2.,,,...,.... 1) (38 ) (,, ), 2) 10 ( ), 10. 1) i), ii) (Respiratory distress syndrome), iii), WHO. WHO, 26%, 96%.. (ELISA, IFA), RT-PCR,. ( 21 ), 4. RT-PCR ( ), 2 2. RNA real-time RT-PCR... X,.. X chest CT. CT,,,. SARS ribavirin, steroids, interferon, convalescent plasma, lopinavir/ritonavir,

6 ,. Ribavirin SARS-CoV [13]. lopinavir in vitro [14]. Interferon X, [15].,,,,,. polyprotein [16], SARS-CoA genome replicase 1A region interfering RNA in vitro SARS-CoV. spike glycoprotein(s1). spike protein C peptide-1(cp-1) SARS-CoV.. [6]...,,,...,...,, WHO,,..., N ,.., Abraham T. ed. Twenty-First Century Plaque. The Story of SARS. Baltimore: The Johns Hopkins University Press, 2005: Smolinski MS, Hamburg MA, Lederberg J. eds. Microbial Threats to Health: Emergence, Detection, Response. Washington, D.C.: National Academic Press, 2003; Update: Outbreak of Severe Acute Respiratory Syndrome-Worldwide,2003.MMWR 2003;52: World Health Organization. Summary of probable SARS cases with onset of illness from 1 November 2002 to 31 July 2003;26 September sars/country/table2003_09_23/en/[online] 5. Peris JS, Yuen KY, Ostehaus, ADME, Stoehr KS. The Severe Acute Respiratory Syndrome. N Engl J Med. 2003;349: Jung EK. SARS management in Korea. Communicable

7 Diseases Monthly Report November 2003 DMR. dyear=2003 &cdmonth=11&cdpart=1&cdmrno=589[online] 7. Drosten C, Gunther S, Preiser W, van der Werf S, Brodt HR, Becker S, et al. : Identification of a novel coronavirus in patients with severe acute respiratory syndrome. N Engl J Med 2003;348(20): Ksiazek TG, Erdman D, Goldsmith CS, Zaki SR, Peret T, Emery S, et al. A novel coronavirus associated with severe acute respiratory syndrome. N Engl J Med 2003;348 (20): Poutanen SM and Low DE. Severe Acute Respiratory Syndrome: an update Current Opinion in Infectious Disease 2004;17: The Chinese SARS Molecular Epidemiology Consortium. Molecular evolution of the SARS coronavirus during the course of the SARS epidemic in China. Science 2004;303; Riley S, Fraser C, Donnelly CA, Ghani AC, Abu-Raddad LJ, Hedley AJ, et al. Transmission dynamics of the etiological agent of SARS in Hong Kong: impact of public health intervention. Science 2003;300: Shen Z, Ning F, Zhou W, He X, Lin C, Chin DP, et al. Superspreading SARS events, Beijing, Emerg Infect Dis 2004;10: Stroher U, DiCaro A, Li Y, Strong JE, Aoki F, Plummer F, et al. Severe acute respiratory syndrome-related coronavirus is inhibited by interferon-alpha. J Infec Dis 2004;189; Chan KS, Lai ST, Chu CM, Tsui E, Tam CY, Wong MM, et al. Treatment of severe acute respiratory syndrome with lopinavir/ritonavir: a multicentre retrospective matched cohort study. Hong Kong Med J 2003;9: Loutfy MR, Blatt LM, Siminovitch KA, Ward S, Wolff B, Lho H, et al. Interferon alfacon-1 plus corticosteroids in severe acute respiratory syndrome. JAMA 2003;290: Anand K, Ziebuhr J, Wadhwani P, Mesters JR, Hilgenfeld R. Coronavirus main proteinase (3CLpro) structure: basis for design of anti-sars drugs. Science. 2003;300:

8 Severe Acute Respiratory Syndrome, SARS Do-Young Song 1, and Won-Kil Lee 2 Department of Laboratory Medicine, Taegu Fatima Hospital 1, and Department of Laboratory Medicine, Kyungpook National University School of Medicine 2, Taegu, Korea An international outbreak of severe acute respiratory syndrome (SARS), a recently recognized syndrome caused by the newly identified severe acute respiratory syndrome-associated coronavirus (SARS-CoV), began in November 2002 and ended in July Coronavirus is a family of enveloped, single stranded-rna viruses causing disease in humans and animals, but the other known coronaviruses that affect humans cause only the common cold. The number of SARS cases in 2003 was approximately 8000 across the world. Many recent studies have reinforced initial impressions that SARS-CoV is primarily transported via contact and/or droplets and that the combination of standard, contact, and droplet precautions is generally effective for its control. Active surveillance for clusters of cases of severe respiratory disease must be a first priority, especially among health care workers. Such surveillance should include the rapid diagnosis and prevention of other respiratory viruses that cause outbreaks of febrile respiratory disease-notably, influenza. Surveillance on the part of clinicians is the key to the early detection of any reemergence before it regains a foothold in the community. During the outbreak of SARS, ribavirin, steroids, interferon, convalescent plasma, and lopinavir/ itonavir were used in varying doses and combinations in different regions of the world. At present no definitive conclusions regarding the efficacy of any of these treatments can be drawn. New findings regarding SARS are continuing to be discovered at an unprecedented pace, permitting a better understanding of the disease and enabling better preparation for its possible returns. Severe Acute Respiratory Syndrome(SARS), Coronavirus, Surveillance, World Health Organization(WHO) Address reprint requests to : Do-Young Song, M.D., Department of Laboratory Medicine, Taegu Fatima Hospital , Sinam-Dong, Dong-Gu, Taegu , Korea. Tel Fax songdy@hitel.net

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°Ç°�°úÁúº´6-2È£ K O R E A C E N T E R S F O R D I S E A S E C O N T R O L & P R E V E N T I O N PHWR Vol. 6 No. 2 www.cdc.go.kr 2013 1 11 6 2 ISSN:2005-811X Flavivirus surveillance in mosquitoes collected from the quarantine