SARS-CoV

SARSコロナウイルス

WordNet

1. the 3rd letter of the Roman alphabet (同)c
2. (music) the keynote of the scale of C major
3. a general-purpose programing language closely associated with the UNIX operating system
4. Nazi militia created by Hitler in 1921 that helped him to power but was eclipsed by the SS after 1943 (同)Sturmabteilung, Storm Troops

PrepTutorEJDIC

1. carbonの化学記号
2. cobaltの化学記号

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/08/12 16:35:09」(JST)

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Coronavirus
Virus classification
Group:	Group IV ((+)ssRNA)
Order:	Nidovirales
Family:	Coronaviridae
Subfamily:	Coronavirinae
Genus:	Betacoronavirus
Species:	SARS coronavirus

The SARS coronavirus, sometimes shortened to SARS-CoV, is the virus that causes severe acute respiratory syndrome (SARS). In April 16 of 2003, following the outbreak of SARS in Asia and secondary cases elsewhere in the world, the World Health Organization (WHO) issued a press release stating that the coronavirus identified by a number of laboratories was the official cause of SARS. Samples of the virus are being held in laboratories in New York, San Francisco, Manila, Hong Kong, and Toronto.

On April 12, 2003, scientists working at the Michael Smith Genome Sciences Centre in Vancouver, British Columbia finished mapping the genetic sequence of a coronavirus believed to be linked to SARS. The team was led by Dr. Marco Marra and worked in collaboration with the British Columbia Centre for Disease Control and the National Microbiology Laboratory in Winnipeg, Manitoba, using samples from infected patients in Toronto. The map, hailed by the WHO as an important step forward in fighting SARS, is shared with scientists worldwide via the GSC website (see below). Dr. Donald Low of Mount Sinai Hospital in Toronto described the discovery as having been made with "unprecedented speed." The sequence of the SARS coronavirus has since been confirmed by other independent groups.

SARS

Main article: Severe acute respiratory syndrome

SARS, or Severe acute respiratory syndrome, is the disease caused by SARS coronavirus. It causes an often severe illness marked initially by systemic symptoms of muscle pain, headache, and fever, followed in 2–10 days by the onset of respiratory symptoms, mainly cough, dyspnea, and pneumonia. Another common finding in SARS patients is a decrease in the number of lymphocytes circulating in the blood.

In the SARS outbreak of 2003, about 9% of patients with confirmed SARS infection died. The mortality rate was much higher for those over 50 years old, with mortality rates approaching 50% for this subset of patients.

Virology

SARS coronavirus is a positive and single stranded RNA virus belonging to a family of enveloped coronaviruses. Its genome is about 29.7kb, which is one of the largest among RNA viruses. The SARS virus has 13 known genes and 14 known proteins. There are 265bp in the 5'UTR and 342bp in the 3'UTR. SARS is similar to other coronaviruses in that its genome expression starts with translation of two large ORFs 1a and 1b, which are two polyproteins.

The functions of several of these proteins are known: ORFs 1a and 1b encode the replicase and there are four major structural proteins: nucleocapsid, spike, membrane and envelope. It also encodes for eight unique proteins, known as the accessory proteins, with no known homologues. The function of these accessory proteins remains unknown.

Coronaviruses usually express pp1a (the ORF1a polyprotein) and the PP1ab polyprotein with joins ORF1a and ORF1b. The polyproteins are then processed by enzymes that are encoded by ORF1a. Product proteins from the processing includes various replicative enzymes such as RNA dependent polymerase, RNA helicase, and proteinase. The replication complex in coronavirus is also responsible for the synthesis of various mRNAs downstream of ORF 1b, which are structural and accessory proteins. Two different proteins, 3CLpro and PL2pro, cleave the large polyproteins into 16 smaller subunits.

SARS-Coronavirus follows the replication strategy typical of the Coronavirus genus.

Morphology

The morphology of the SARS coronavirus is characteristic of the coronavirus family as a whole. These viruses have large pleomorphic spherical particles with bulbous surface projections that form a corona around particles. The envelope of the virus contains lipid and appears to consist of a distinct pair of electron dense shells.

The internal component of the shell is a single-stranded helical ribonucleoprotein. There are also long surface projections that protrude from the lipid envelop. The size of these particles are about 80–90 nm.

Viral replication

Coronavirus (CoV) genome replication takes place in the cytoplasm in a membrane-protected microenvironment and starts with the translation of the genome to produce the viral replicase. CoV transcription involves a discontinuous RNA synthesis during the extension of a negative copy of the subgenomic mRNAs. The requirement for base pairing during transcription has been formally demonstrated in arteriviruses and CoVs. The CoV N protein is required for coronavirus RNA synthesis and has RNA chaperon activity that may be involved in template switch. Both viral and cellular proteins are required for replication and transcription. CoVs initiate translation by cap-dependent and cap-independent mechanisms. Cell macromolecular synthesis may be controlled after CoV infection by locating some virus proteins in the host cell nucleus. Infection by different coronaviruses cause in the host alteration in the transcription and translation patterns, in the cell cycle, the cytoskeleton, apoptosis and coagulation pathways, inflammation and stress responses. The balance between genes up- and down-regulated could explain the pathogenesis caused by these viruses. Coronavirus expression systems based on single genome constructed by targeted recombination, or by using infectious cDNAs, have been developed. The possibility of expressing different genes under the control of transcription regulating sequences (TRSs) with programmable strength and engineering tissue and species tropism indicates that CoV vectors are flexible. CoV based vectors have emerged with high potential vaccine development and possibly for gene therapy.

Evolution

SARS is most closely related to group 2 coronaviruses, but it does not segregate into any of the other three groups of coronaviruses. The closest outgroup to the coronaviruses are the toroviruses, with which it has homology in the ORF 1b replicase and the two viron proteins of S and M. SARS was determined to be an early split off from the group 2 coronaviruses based on a set of conserved domains that it shares with group 2.

A main difference between group 2 coronovirus and SARS is the nsp3 replicase subunit encoded by ORF1a. SARS does not have a papain-like proteinase 1.

Symptoms and treatment

Once a person has contracted SARS, the first symptom that they present with is a fever of at least 38°C (100.4°F) or higher. The early symptoms last about 2–7 days and include non-specific flu-like symptoms, including chills/rigor, muscle aches, headaches, diarrhea, sore throat, runny nose, malaise, and myalgia (muscle pain). Next, they develop a dry cough, shortness of breath, and an upper respiratory tract infection.

At that time, a chest x-ray is ordered to confirm pneumonia. If the chest appears clear and SARS is still suspected, a HRCT scan will be ordered, because it is visible earlier on this scan. In severe cases, it develops into respiratory failure and acute respiratory distress syndrome (ARDS), and in 70-90% of the cases, they develop lymphopenia (low count of lymphocyte white blood cells).

The incubation period for SARS-CoV is from 2–10 days, sometimes lasting up to 13 days, with a mean of 5 days. So symptoms usually develop between 2–10 days following infection by the virus. As part of the immune response, IgM antibody to the SARS-CoV is produced. This peaks during the acute or early convalescent phase (week 3) and declines by week 12. IgG antibody is produced later and peaks at week 12.

Engineering the virus

Engineering of SARS virus has been done. In a paper published in 2006, a new transcription circuit was engineered to make recombinant SARS viruses. The recombination allowed for efficient expression of viral transcripts and proteins. The engineering of this transcription circuit reduces the RNA recombinant progeny viruses. The TRS (transcription regulatory sequences) circuit regulates efficient expression of SARS-CoV subgenomic mRNAs. The wild type TRS is ACGAAC.

A double mutation results in TRS-1 (ACGGAT) and a triple mutation results in TRS-2 (CCGGAT). When the remodeled TRS circuit containing viruses are genetically recombined with wild type TRS circuits, the result is a circuit reduced in production of subgenomic mRNA. The goal of modifying the SARS virus with this approach is to produce chimeric progeny that have reduced viability due to the incompatibility of the WT and engineered TRS circuits.

Novel subunit vaccine constructs for an S protein SARS vaccine based on the receptor binding domain (RBD) are being developed by the New York Blood Center. The re-emergence of SARS is possible, and the need remains for commercial vaccine and therapeutic development. However, the cost and length of time for product development, and the uncertain future demand, result in unfavorable economic conditions to accomplish this task. In the development of therapeutics and next-generation vaccines, more work is required to determine the structure/ function relationships of critical enzymes and structural proteins.

See also

• Carlo Urbani
• Progress of the SARS outbreak
• Severe acute respiratory syndrome

Notes

References

• J S M Peiris et al. (5 April 2003). "Coronavirus as a possible cause of severe acute respiratory syndrome" (PDF). The Lancet 361 (9364). 

• Paul A. Rota et al. (30 May 2003). "Characterization of a Novel Coronavirus Associated with Severe Acute Respiratory Syndrome". Science 300 (5624): 1394–1399. doi:10.1126/science.1085952. PMID 12730500. . Published online 1 May 2003; doi:10.1126/science.1085952

• Marco A. Marra et al. (30 May 2003). "The Genome Sequence of the SARS-Associated coronavirus". Science 300 (5624): 1399–1404. doi:10.1126/science.1085953. PMID 12730501. . Published online 1 May 2003; doi:10.1126/science.1085953

• Snijder EJ et al. (29 August 2003). "Unique and conserved features of genome and proteome of SARS-coronavirus, an early split-off from the coronavirus group 2 lineage". J Mol Biol 331 (5): 991–1004. doi:10.1016/S0022-2836(03)00865-9. PMID 12927536. 

• Yount B et al. (15 August 2006). "Rewiring the severe acute respiratory syndrome coronavirus (SARS-CoV) transcription circuit: engineering a recombination-resistant genome". Proc Natl Acad Sci U S A 103 (33): 12546–51. doi:10.1073/pnas.0605438103. PMC 1531645. PMID 16891412. 

• Thiel V (editor). (2007). Coronaviruses: Molecular and Cellular Biology (1st ed.). Caister Academic Press. ISBN 978-1-904455-16-5. 

• Enjuanes L, et al. (2008). "Coronavirus Replication and Interaction with Host". Animal Viruses: Molecular Biology. Caister Academic Press. ISBN 978-1-904455-22-6. 

External links

• WHO press release identifying and naming the SARS virus
• The SARS virus genetic map
• Science special on the SARS virus (free content: no registration required)
• McGill University SARS Resources (From web archive)
• U.S. Centers for Disease Control and Prevention (CDC) SARS home
• World Health Organization on alert

UpToDate Contents

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• 1. 重症急性呼吸器症候群（SARS） severe acute respiratory syndrome sars
• 2. コロナウイルス coronaviruses
• 3. 東アジアへの旅行によって感染する可能性のある疾患 diseases potentially acquired by travel to east asia
• 4. 東南アジアへの旅行によって感染する可能性のある疾患 diseases potentially acquired by travel to southeast asia
• 5. 小児における肺炎の疫学、病因、および原因 epidemiology pathogenesis and etiology of pneumonia in children

English Journal

• Yeast-based assays for the high-throughput screening of inhibitors of coronavirus RNA cap guanine-N7-methyltransferase.

• Sun Y1, Wang Z1, Tao J1, Wang Y1, Wu A1, Yang Z2, Wang K2, Shi L2, Chen Y3, Guo D4.Author information 1State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, PR China.2Biological Pesticide Engineering Research Center, Hubei Academy of Agricultural Science, Hubei 430072, PR China.3State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, PR China. Electronic address: chenyu@whu.edu.cn.4State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, PR China. Electronic address: dguo@whu.edu.cn.AbstractThe 5'-cap structure is a distinct feature of eukaryotic mRNAs and is important for RNA stability and protein translation by providing a molecular signature for the distinction of self or non-self mRNA. Eukaryotic viruses generally modify the 5'-end of their RNAs to mimic the cellular mRNA structure, thereby facilitating viral replication in host cells. However, the molecular organization and biochemical mechanisms of the viral capping apparatus typically differ from its cellular counterpart, which makes viral capping enzymes attractive targets for drug discovery. Our previous work showed that SARS coronavirus (SARS-CoV) non-structural protein 14 represents a structurally novel and unique guanine-N7-methyltransferase (N7-MTase) that is able to functionally complement yeast cellular N7-MTase. In the present study, we developed a yeast-based system for identifying and screening inhibitors against coronavirus N7-MTase using both 96-well and 384-well microtiter plates. The MTase inhibitors previously identified by in vitro biochemical assays were tested, and some, such as sinefungin, effectively suppressed N7-MTase in the yeast system. However, other compounds, such as ATA and AdoHcy, did not exert an inhibitory effect within a cellular context. These results validated the yeast assay system for inhibitor screening yet also demonstrated the difference between cell-based and in vitro biochemical assays. The yeast system was applied to the screening of 3000 natural product extracts, and three were observed to more potently inhibit the activity of coronavirus than human N7-MTase.
• Antiviral research.Antiviral Res.2014 Apr;104:156-64. doi: 10.1016/j.antiviral.2014.02.002. Epub 2014 Feb 11.
• The 5'-cap structure is a distinct feature of eukaryotic mRNAs and is important for RNA stability and protein translation by providing a molecular signature for the distinction of self or non-self mRNA. Eukaryotic viruses generally modify the 5'-end of their RNAs to mimic the cellular mRNA structure
• PMID 24530452

• The ORF4a protein of human coronavirus 229E functions as a viroporin that regulates viral production.

• Zhang R1, Wang K2, Lv W2, Yu W2, Xie S2, Xu K2, Schwarz W3, Xiong S4, Sun B5.Author information 1Jiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, China; Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, China.2Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, China.3Goethe-University Frankfurt, Institute for Biophysics, Max-von-Laue-Str. 1, D-60438 Frankfurt am Main, Germany; Shanghai Research Center for Acupuncture and Meridian, 199 Guoshoujing Road, Shanghai 201023, China.4Jiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, China. Electronic address: sdxiongfd@126.com.5Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200025, China; State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China. Electronic address: bsun@sibs.ac.cn.AbstractIn addition to a set of canonical genes, coronaviruses encode additional accessory proteins. A locus located between the spike and envelope genes is conserved in all coronaviruses and contains a complete or truncated open reading frame (ORF). Previously, we demonstrated that this locus, which contains the gene for accessory protein 3a from severe acute respiratory syndrome coronavirus (SARS-CoV), encodes a protein that forms ion channels and regulates virus release. In the current study, we explored whether the ORF4a protein of HCoV-229E has similar functions. Our findings revealed that the ORF4a proteins were expressed in infected cells and localized at the endoplasmic reticulum/Golgi intermediate compartment (ERGIC). The ORF4a proteins formed homo-oligomers through disulfide bridges and possessed ion channel activity in both Xenopus oocytes and yeast. Based on the measurement of conductance to different monovalent cations, the ORF4a was suggested to form a non-selective channel for monovalent cations, although Li(+) partially reduced the inward current. Furthermore, viral production decreased when the ORF4a protein expression was suppressed by siRNA in infected cells. Collectively, this evidence indicates that the HCoV-229E ORF4a protein is functionally analogous to the SARS-CoV 3a protein, which also acts as a viroporin that regulates virus production. This article is part of a Special Issue entitled: Viral Membrane Proteins - Channels for Cellular Networking.
• Biochimica et biophysica acta.Biochim Biophys Acta.2014 Apr;1838(4):1088-95. doi: 10.1016/j.bbamem.2013.07.025. Epub 2013 Jul 29.
• In addition to a set of canonical genes, coronaviruses encode additional accessory proteins. A locus located between the spike and envelope genes is conserved in all coronaviruses and contains a complete or truncated open reading frame (ORF). Previously, we demonstrated that this locus, which contai
• PMID 23906728

• SARS coronavirus papain-like protease inhibits the type I interferon signaling pathway through interaction with the STING-TRAF3-TBK1 complex.

• Chen X1, Yang X, Zheng Y, Yang Y, Xing Y, Chen Z.Author information 1Division of Infection and Immunity, Department of Electromagnetic and Laser Biology, Beijing Institute of Radiation Medicine, Beijing, 100850, China.AbstractSARS coronavirus (SARS-CoV) develops an antagonistic mechanism by which to evade the antiviral activities of interferon (IFN). Previous studies suggested that SARS-CoV papain-like protease (PLpro) inhibits activation of the IRF3 pathway, which would normally elicit a robust IFN response, but the mechanism(s) used by SARS PLpro to inhibit activation of the IRF3 pathway is not fully known. In this study, we uncovered a novel mechanism that may explain how SARS PLpro efficiently inhibits activation of the IRF3 pathway. We found that expression of the membrane-anchored PLpro domain (PLpro-TM) from SARS-CoV inhibits STING/TBK1/IKKε-mediated activation of type I IFNs and disrupts the phosphorylation and dimerization of IRF3, which are activated by STING and TBK1. Meanwhile, we showed that PLpro-TM physically interacts with TRAF3, TBK1, IKKε, STING, and IRF3, the key components that assemble the STING-TRAF3-TBK1 complex for activation of IFN expression. However, the interaction between the components in STING-TRAF3-TBK1 complex is disrupted by PLpro-TM. Furthermore, SARS PLpro-TM reduces the levels of ubiquitinated forms of RIG-I, STING, TRAF3, TBK1, and IRF3 in the STING-TRAF3-TBK1 complex. These results collectively point to a new mechanism used by SARS-CoV through which PLpro negatively regulates IRF3 activation by interaction with STING-TRAF3-TBK1 complex, yielding a SARS-CoV countermeasure against host innate immunity.
• Protein & cell.Protein Cell.2014 Mar 14. [Epub ahead of print]
• SARS coronavirus (SARS-CoV) develops an antagonistic mechanism by which to evade the antiviral activities of interferon (IFN). Previous studies suggested that SARS-CoV papain-like protease (PLpro) inhibits activation of the IRF3 pathway, which would normally elicit a robust IFN response, but the mec
• PMID 24622840

Japanese Journal

• Synthesis of Bioactive Natural Products as Protein Inhibitors

• KONNO Hiroyuki
• Bioscience, biotechnology, and biochemistry 76(7), 1257-1261, 2012-07-23
• NAID 10030981537

• Design, Synthesis and Evalution of Tripeptidomimetics with Arylketone as Inhibitors of SARS-CoV 3CL Protease

• KONNO Sho,NAKADA Kiyohiko,THANIGAIMALAI Pillaiyar,KAKIUCHI Rie,YAMAMOTO Takehito,YAMAZAKI Yuri,YAKUSHIJI Fumika,AKAJI Kenichi,KISO Yoshiaki,KAWASAKI Yuko,FRIERE Ernest,HAYASHI Yoshio
• Peptide science : proceedings of the ... Japanese Peptide Symposium 2011, 151-154, 2012-03-01
• NAID 10030204179

• Diarylheptanoids from Alnus japonica Inhibit Papain-Like Protease of Severe Acute Respiratory Syndrome Coronavirus

• Park Ji-Young,Jae Jeong Hyung,Hoon Kim Jang,Min Kim Young,Park Su-Jin,Kim Doman,Hun Park Ki,Song Lee Woo,Bae Ryu Young
• Biological and Pharmaceutical Bulletin 35(11), 2036-2042, 2012
• … The papain-like protease (PLpro), which controls replication of the severe acute respiratory syndrome coronavirus (SARS-CoV), has been identified as a potential drug target for the treatment of SARS. … An intensive hunt for effective anti-SARS drugs has been undertaken by screening for natural product inhibitors that target SARS-CoV PLpro. …
• NAID 130001872274

Related Links

• SARSコロナウイルス - Wikipedia

SARSコロナウイルス（サーズコロナウイルス）（英: SARS coronavirus,SARS-CoV）は 、重症急性呼吸器症候群 (Severe Acute Respiratory Syndrome, SARS) の病原体 として同定された新種のコロナウイルスである。通称SARSウイルス。飛沫感染により ...

• SARS coronavirus - Wikipedia, the free encyclopedia

The SARS coronavirus, sometimes shortened to SARS-CoV, is the virus that causes severe acute respiratory syndrome (SARS). In April 16 of 2003, following the outbreak of SARS in Asia and secondary cases elsewhere in the world, the ...

Related Pictures

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★リンクテーブル★

リンク元	「重症急性呼吸器症候群」「SARS coronavirus」「SARS virus」「SARS-associated coronavirus」
拡張検索	「SARS-CoV-2」「SARS-CoV-1」
関連記事	「C」「SA」「SARS」「SAR」「Co」

「重症急性呼吸器症候群」

　　[★]

英

severe acute respiratory syndrome SARS

関

コロナウイルス。SARSコロナウイルス(SARS-CoV-1)

概念

• SARSコロナウイルス(SARS-CoV-1)の感染に起因する急性呼吸促迫症候群(ARDS)である。
• 2003年一類感染症に指定されたが、2020年現在は二類感染症に分類されている

歴史

• 2002年11月から2003年2月まで中国広東省に多数の感染者が発生し、香港、ハノイ、カナダ、シンガポール台湾で感染が拡大

病原体

• SARSウイルス SARS-CoV

• 新型のコロナウイルス

感染経路

• 飛沫感染　　空気感染ではない
• 病初期にウイルスの排出量は少ない
• ACE2受容体を介して感染が成立する

潜伏期

• 通常2-10日(平均6日、中央値4-5日)。

症状

• 38℃以上の発熱、悪寒、筋肉痛、頭痛、倦怠感などのインフルエンザ様症状で発症する。
• 発症後3-7日後に、乾性咳嗽、呼吸困難などの下気道症状が

咳嗽、呼吸困難、頭痛、下痢、全身倦怠感など

• 約20%の例で重篤な呼吸不全に陥る。

感染症専門医テキスト 第1部 解説編

	香港	香港	シンガポール	トロント
	Peiris,et al	Lee,et al	Hsu,et al	Booth,et al
	(n=50)	(n=138)	(n=20)	(n=144)
発熱	100	100	100	99.3
悪寒	74	73.2	15	27.8
筋肉痛	54	60.9	45	49.3
咳嗽	62	57.3	75	69.4
呼吸因難	20	ー	40	41.7
頭痛	20	55.8	20	35.4
めまい	12	42.8	ー	4.2
喀痰	ー	29	ー	4.9
下痢	10	19.6	25	23.6
悪心,嘔吐	20	19.6	35	19.4
咽頭痛	20	23.2	25	12.5
倦怠感	50	ー	45	31.2

検査

• 血液検査：リンパ球・血小板数減少、APTT延長、LDH・CPK・トランスアミナーゼ上昇が見られる
• 胸部CT：ARDS様のスリガラス影

鑑別疾患

• インフルエンザウイルスによる肺炎、マイコプラズマ肺炎、クラミジア肺炎

予後

• 致死率：10%
• 基礎疾患を有するものや65歳以上では予後が不良である。
• 小児は相対的に予後が良好

「SARS coronavirus」

　　[★]

• SARSコロナウイルス

関

SARS virus、SARS-associated coronavirus、SARS-CoV

「SARS virus」

　　[★]

SARSウイルス

関

SARS coronavirus、SARS-associated coronavirus、SARS-CoV

「SARS-associated coronavirus」

　　[★]

• SARS関連コロナウイルス

関

SARS coronavirus、SARS virus、SARS-CoV

「SARS-CoV-2」

　　[★]

同

新型コロナウイルス

関

コロナウイルス。COVID-19

概念

• ニドウイルス目 Nidovirales コロナウイルス科 Coronaviridae コロナウイルス属に所属するウイルスである。
• コロナウイルスは4種の血清型を有しており、SARS-CoV-2はβコロナウイルスに所属し、SARSコロナウイルス,MERSコロナウイルス,OC43株,HKU1株と同じ属である。
• ヒト細胞への感染はACE2をレセプターとすることが明らかになっており、これはSARSコロナウイルスやNK63株と同じである。
• 2019年12月末に中国湖北省武漢市で新型コロナウイルスのヒトへの感染が認められ、中国全土に拡大した。後に新型コロナウイルスはSARS-CoV-2と名付けられ、これによる感染症はCOVID-19と命名された。

「SARS-CoV-1」

　　[★]

関

SARSコロナウイルス、重症急性呼吸器症候群

• ニドウイルス目 Nidovirales コロナウイルス科 Coronaviridae コロナウイルス属 βコロナウイルスに所属している。

「C」

　　[★]

• 炭素 carbon
• シトシン cytosine
• システイン cysteine
• シチジン
• セルシウス度 摂氏 degrees Celsius degree C
• 産婦人科領域で「子宮外頚 子宮外頚部 exocervix」を表現するための略語

　 　 　 　

「SA」

　　[★]

• 鉄芽球性貧血 sideroblastic anemia
• シアル酸
• 自然流産 spontaneous abortion

　

「SARS」

　　[★] 重症急性呼吸器症候群 severe acute respiratory syndrome

「SAR」

　　[★]

同

seasonal allergic rhinitis

「Co」

　　[★] コバルト cobalt