Pathogen Safety Data Sheets: Infectious Substances – Severe acute respiratory syndrome (SARS) associated coronavirus

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Section I - Infectious agent

Name: Severe acute respiratory syndrome (SARS)-related coronavirus
Agent type: Virus


Family: Coronaviridae
Genus: Betacoronavirus
Species: Severe acute respiratory syndrome-related coronavirus
Synonym or cross reference: SARS-CoV Footnote 1Footnote 2Footnote 3, SCV Footnote 3, SCoV Footnote 4, CoV Footnote 5, formerly "atypical pneumonia" in China before SARS was identified Footnote 2Footnote 6Footnote 7Footnote 8Footnote 9Footnote 10. Footnote 9Footnote 10


Brief description: First isolated in 2003 Footnote 7Footnote 8, and originating from Guangdon province of southern China, SARS-CoV is a novel coronavirus that is phylogenetically distinct and only distantly related to other human coronaviruses Footnote 6Footnote 9. SARS-CoV is a spherical enveloped virion measuring 80 to 140 nm in diameter Footnote 1Footnote 7, with a single-stranded, linear, non-segmented, positive-sense RNA genome 30 kb in size Footnote 1Footnote 2Footnote 9Footnote 11.

Properties: Unlike most coronaviruses with narrow host ranges, SARS-CoV is able to infect cell cultures other than the natural host species and closely related species Footnote 6Footnote 9.

Section II - Hazard identification

Pathogenicity and toxicity: Most common initial symptoms include a fever greater than 38°C Footnote 1Footnote 2, often accompanied by myalgia, malaise, chills, headache, diarrhea, a non-productive cough, shortness of breath, and rigor Footnote 1Footnote 7Footnote 8Footnote 12. After 2 to 7 days, this is followed by respiratory symptoms such as a dry cough, shortness of breath, difficulty breathing, or hypoxia Footnote 1Footnote 2Footnote 12. In some cases, the respiratory symptoms become increasingly severe, and patients require oxygen support and mechanical ventilation Footnote 1Footnote 12. Similar to other cases of atypical pneumonia, physical signs upon chest examination are minimal compared with radiological findings, which typically show ground-glass opacities and focal consolidations Footnote 1. Diarrhea is the most common extra-pulmonary manifestation Footnote 13, followed by hepatic dysfunction, dizziness, abnormal urinalysis, petechiae, myositis, neuromuscular abnormalities, and epileptic fits Footnote 1. The case-fatality rate is 9.6% Footnote 2Footnote 12Footnote 14; however, in patients over 65 years of age, this rate exceeds 50% Footnote 6Footnote 12Footnote 15. Attack rates, defined as the proportion of those who become ill in an exposed population initially free from disease, of over 50% have been reported in hospitals Footnote 16Footnote 17. While infections in children appear to be milder than those in adults Footnote 18, SARS in pregnant women carries a significant risk of mortality Footnote 19Footnote 20.

Since coronavirus infection is generally host-specific, natural animal hosts do not reportedly display overt signs of disease when infected with SARS-CoV Footnote 4Footnote 21Footnote 22. Animal pathogenicity is derived mainly from experimental data. Animal models infected with human isolates of SARS-CoV experience less severe symptoms of disease such as mild lung pathology, lethargy, fever, diarrhea, and conjunctivitis, with some animals recovering on their own Footnote 3Footnote 21Footnote 23Footnote 24. Respiratory distress and temporary skin rash have also been reported in a few experimentally infected Rhesus macaques Footnote 21. Although coronavirus infection in domestic animals does occur, experimental infection with a SARS-CoV human isolate did not produce clinical signs of disease or pathology in pigs, chickens, geese, Pekin ducks, turkeys, or quail despite viral RNA detection in swab specimens, and blood and tissue samples Footnote 25Footnote 26.

Predisposing factors: Pregnant women Footnote 20 and those 65 years or older Footnote 6Footnote 15 are at an increased risk of more severe disease.

Communicability: Person-to-person transmission (direct mucous membrane contact (eyes, nose, and mouth) with infectious respiratory droplets and/or direct contact with infected body fluids) and/or through exposure to contaminated fomites Footnote 7Footnote 10Footnote 27Footnote 28. The virus preferably spreads via respiratory droplets over a close distance Footnote 27Footnote 29. Other possible modes of transmission include through inhalation of infectious aerosols, blood transfusions, or by sharps injuries Footnote 27Footnote 28. Communicability is at its greatest in severely ill patients or those experiencing rapid clinical deterioration. Transmission usually occurs after onset of clinical signs and symptoms (on or after the 5th day of illness on average), which coincides with peak viral load in nasopharyngeal secretions around the 10th day of illness Footnote 1Footnote 12Footnote 13. The maximum period of communicability is 21 days Footnote 12.

Non-inoculated cats housed with experimentally infected cats and ferrets also became infected with SARS-CoV, although no elaboration was provided on the possible mode of transmission Footnote 3. Mice, golden hamsters, and non-human primates have been used to study SARS-CoV infection but virus transmission within members of the same species or between these animal models has not been reported Footnote 30.

Epidemiology: SARS-CoV is a novel virus that caused the first major pandemic of the new millennium Footnote 7Footnote 8Footnote 31. The earliest known cases were identified in mid-November 2002 in the Guangdong Province of South-East China Footnote 5Footnote 6Footnote 32. The index case was reported in Foshan, a city 24 km from Guangzhou Footnote 1Footnote 5. Retrospective analysis revealed severe cases of the disease in 5 cities around Guangzhou over a period of 2 months, with many of the cases having had epidemiological links to the live-animal market trade Footnote 5. A serological study on the prevalence of antibodies to SARS-CoV in civets from the Xinyuan Live Animal Market in Guangzhou and farms in different regions of Guangdong, Henan, and Hunan Provinces was performed. The results revealed a seroprevalence of 78% in the Xinyuan Live Animal Market, compared to an overall prevalence of ~10% for farms in the various regions, pointing towards a specific outbreak originating in Guangzhou Footnote 33.

Subsequent to its introduction to Hong Kong in mid-February 2003, the virus spread to Vietnam, Singapore, Canada, the Philippines, the United Kingdom, the United States, and then back again to China Footnote 1. By the end of July 2003, SARS had spread to affect a reported 8,098 people in over 30 countries, across 5 continents, killing 774 people Footnote 2Footnote 14Footnote 31. Over half of these infections can be traced back to 1 index patient who arrived in Hong Kong on February 21, 2003, and 21% of all cases were healthcare workers Footnote 14Footnote 31. Although the World Health Organization declared the end of the SARS epidemic in early July 2003, sporadic outbreaks of SARS occurred in late 2003 and early 2004, due to laboratory incidents Footnote 34Footnote 35Footnote 36, and community-acquired SARS in the city of Guangzhou, China Footnote 37.

Host range

Natural host(s): Natural hosts include humans, Himalayan palm civets (Paguma larvata), racoon dogs (Nyctereutes procyonoides), Chinese ferret badgers (Melogale moschata), cats, and pigs Footnote 3Footnote 4Footnote 38Footnote 39.

Other host(s): Experimental hosts include non-human primates, poultry, ferrets, golden hamsters, guinea pigs, mice, and rats Footnote 25Footnote 26Footnote 38.

Infectious dose: Experimental infection with 105 PFU of recombinant mouse-adapted SARS-CoV in mice resulted in development of significant clinical disease including labored breathing and death Footnote 40. In another study, 107 PFU of recombinant SARS-CoV isolates obtained from human and zoonotic strains Footnote 41 were inoculated in cynomolgus macaques, producing radiological changes without development of overt clinical symptoms Footnote 42; however, the precise infectious dose remains unknown for humans and animals alike.

Incubation period: The incubation period of SARS ranges from 2 to 16 days, with a maximum of 10 days as the best estimate Footnote 2Footnote 6Footnote 15. The rate of viral shedding from nasopharynx, stool, and urine samples progressively declines from day 10 to 21 after onset of symptoms Footnote 13. The viral load in nasopharyngeal secretions peaks around day 10 Footnote 1Footnote 12.

Section III - Dissemination

Reservoir: Bats are the origin and natural reservoir for SARS-CoV Footnote 43. Research is ongoing to identify the specific reservoir species, although the Chinese Horseshoe Bat (Rhinolophus spp.) is considered the most likely candidate since SARS-CoV-like viruses having a high degree of sequence homology with SARS-CoV were found in these animals Footnote 38Footnote 39Footnote 44Footnote 45Footnote 46. On the other hand, the horseshoe bat angiotensin-converting enzyme 2 (ACE2) was found in one study to be unable to act as a receptor for human SARS-CoV, unlike its human equivalent Footnote 47Rhinolophus sinicus (Chinese Rufous Horseshoe Bat) and Myotis daubentoni (Daubenton's Bat) were found to be susceptible to SARS-CoV infection in this same study.

Zoonosis/Reverse zoonosis: Yes, most likely from Himalayan palm civets (Paguma larvata) to humans Footnote 4Footnote 38. Progenitor SARS-CoV in the bat reservoir is unlikely to be able to infect humans. Rapid viral evolution in an intermediate host, such as the civet, is believed to occur in order for the virus to adapt and infect humans Footnote 38.

Vectors: None.

Section IV - Stability and viability

Drug susceptibility: Unknown.

Drug resistance: Unknown.

Susceptibility to disinfectants: Inactivated by common disinfection measures such as a 5 minute contact with household bleach Footnote 28, ice-cold acetone (90 seconds), ice-cold acetone/methanol mixture (40:60, 10 minutes), 70% ethanol (10 minutes), 100% ethanol (5 minutes), paraformaldehyde (2 minutes), and glutaraldehyde (2 minutes) Footnote 48. Commonly used brands of hand disinfectants also inactivate SARS-CoV (30 seconds) Footnote 48.
Physical inactivation: Sensitive to heat (60°C for 30 minutes) Footnote 48, and UV radiation (60 minutes) Footnote 49.

Survival outside host: Can survive for 4 days in diarrheal stool samples with an alkaline pH Footnote 12Footnote 28Footnote 48, more than 7 days in respiratory secretions at room temperature, for at least 4 days in undiluted urine, feces and human serum at room temperature Footnote 28Footnote 49, up to 9 days in suspension, 60 hours in soil/water, more than a day on hard surfaces such as glass and metal Footnote 48Footnote 49, up to 48 hours on plastic surfaces Footnote 6, and 6 days in dried state Footnote 48. The virus does not survive well after drying on paper, but lasts longer on disposable, compared to cotton, gowns Footnote 28.

Human coronavirus 229E can remain infectious on high-touch environmental surfaces (polyvinylchloride, laminate, wood, stainless steel) for at least 7 days at ambient temperature (24°C) and relative humidity conditions (~50%) Footnote 50. As a human coronavirus with comparable genetic characteristics, SARS-CoV may also survive outside the host under similar conditions.

Section V - First aid/medical

Surveillance: None of the symptoms of SARS can be used to differentiate SARS from other causes of pneumonia or respiratory illness; therefore, laboratory confirmation is the only form of diagnosis Footnote 1Footnote 51. A positive viral culture from a respiratory, fecal, urine, or tissue specimen, or a fourfold rise in neutralising antibody titer taken upon admission and 28 days afterward is the most definitive evidence of SARS infection Footnote 1. Rapid detection of nucleic acid by RT-PCR or antigen by ELISA can be used as alternatives Footnote 34Footnote 52. Immunofluorescence, microneutralisation Footnote 37, electron microscopy, and chest radiography Footnote 18Footnote 31 can also be used to diagnose SARS-CoV. Epidemiological features such as exposure to known SARS case-patients or SARS-affected areas may help in early recognition of infection Footnote 51.

Note: The specific recommendations for surveillance in the laboratory should come from the medical surveillance program, which is based on a local risk assessment of the pathogens and activities being undertaken, as well as an overarching risk assessment of the biosafety program as a whole. More information on medical surveillance is available in the Canadian Biosafety Handbook (CBH).

First aid/treatment: Clinical management of SARS relies largely upon supportive care Footnote 1. Ribavirin, corticosteroids, lopinavir, ritonavir, type 1 interferon, intravenous immunoglobulin, and SARS convalescent plasma have all been used by physicians to treat SARS, but it is not possible to determine whether the treatments actually benefited patients during the SARS outbreak Footnote 53. There are no reports of treatment undertaken for infected animals.

Note: The specific recommendations for first aid/treatment in the laboratory should come from the post-exposure response plan, which should be developed as part of the medical surveillance program. More information on the post-exposure response plan can be found in the CBH.

Immunization: Several inactivated vaccine candidates have been developed but they are not currently available for human use due to major safety concerns Footnote 2. Some vaccines in development have only been tested in animal models without clear evidence of protection from disease Footnote 54. Other vaccines have proven successful in reducing viral replication in animal models; however, these animals do not express all of the clinical signs and lethality of SARS-CoV observed in infected humans Footnote 55Footnote 56.

More information on the medical surveillance program can be found in the CBH, and by consulting the Canadian Immunization Guide.

Prophylaxis: No known post-exposure prophylaxis Footnote 2Footnote 57.

Note: More information on prophylaxis as part of the medical surveillance program can be found in the CBH.

Section VI - Laboratory hazards

Laboratory-acquired infections: Four incidents have been reported to date. The first case occurred in Singapore in September 2003 when a 27 year old graduate student contracted SARS while working with West Nile virus in a culture laboratory where SARS-CoV was being maintained Footnote 34. The second case occurred in December 2003 in Taiwan when a 44 year old researcher contracted the disease while testing herbal remedies against SARS-CoV Footnote 35. The third and fourth cases occurred in China in late-March to mid-April 2004 when 2 CDC workers developed SARS after improperly inactivating a batch of SARS virus in the laboratory Footnote 36. Each case was attributed to poor understanding or lack of safety procedures while working with SARS-CoV.

Please consult the Canadian Biosafety Standard (CBS) and CBH for additional details on requirements and guidelines for reporting exposure incidents.

Sources/specimens: Respiratory secretions, faeces, blood, urine, lung biopsy tissue, and tears of infected individuals Footnote 1Footnote 8Footnote 27Footnote 31Footnote 52.

Primary hazards: Droplet exposure of the mucous membranes of the eye, nose and/or mouth, inhalation of infectious aerosols, and ingestion Footnote 1Footnote 10.

Special hazards: None.

Section VII - Exposure controls/personal protection

Risk group classification: Severe acute respiratory syndrome-related coronavirus is considered to be a Risk Group 3 Human Pathogen Footnote 58 and Risk Group 1 Animal Pathogen. SARS-CoV is a Security Sensitive Biological Agent (SSBA).

Containment requirements: The applicable CL3 requirements outlined in the CBS and in the Biosafety Advisory for Severe Acute Respiratory Syndrome should be followed. Note that there are additional security requirements, such as obtaining a Human Pathogens and Toxins Act Security Clearance, for work involving SSBAs.

Protective clothing: The applicable CL3 requirements for personal protective equipment and clothing outlined in the CBS should be followed.

Based on a local risk assessment, appropriate hand, foot, head, body, eye/face, and respiratory protection should be identified, and the PPE requirements for the containment zone should be documented in Standard Operating Procedures.

Other precautions: All activities involving open vessels of infectious material or toxins to be performed in a certified BSC or other appropriate primary containment device.

Section VIII - Handling and storage

Spills: Allow aerosols to settle. Wearing protective clothing, gently cover the spill with absorbent paper towel and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up.

Disposal: All materials/substances that have come in contact with the infectious agent should be completely decontaminated before they are removed from the containment zone. This can be achieved by using a decontamination method that has been demonstrated to be effective against the infectious material, such as chemical disinfectants, autoclaving, irradiation, incineration, an effluent treatment system, or gaseous decontamination.

Storage: The applicable CL3 requirements for storage outlined in the CBS should be followed. Containers of infectious material or toxins stored outside the containment zone should be labelled, leakproof, impact resistant, and kept in locked storage equipment and within an area with limited access Footnote 59.

Section IX - Regulatory and other information

Regulatory information: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

Work with SARS-CoV requires a Human Pathogens and Toxins Licence, issued by the Public Health Agency of Canada.

Updated: 2018

PREPARED by: Centre for Biosecurity, Public Health Agency of Canada.

Although the information, opinions, and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright©Public Health Agency of Canada, 2019, Canada


Footnote 1

Cheng, V. C. C., S. K. P. Lau, P. C. Y. Woo, and Y. Y. Kwok. 2007. Severe acute respiratory syndrome coronavirus as an agent of emerging and reemerging infection. Clin. Microbiol. Rev. 20:660-694.

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Footnote 2

Feng, Y., and G. F. Gao. 2007. Towards our understanding of SARS-CoV, an emerging and devastating but quickly conquered virus. Comp. Immunol. Microbiol. Infect. Dis. 30:309-327.

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Footnote 3

Martina, B. E. E., B. L. Haagmans, T. Kuiken, R. A. M. Fouchier, G. F. Rimmelzwaan, G. Van Amerongen, J. S. M. Peiris, W. Lim, and A. D. M. E. Osterhaus. 2003. SARS virus infection of cats and ferrets. Nature. 425:915.

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Footnote 4

Guan, Y., B. J. Zheng, Y. Q. He, X. L. Liu, Z. X. Zhuang, C. L. Cheung, S. W. Luo, P. H. Li, L. J. Zhang, Y. J. Guan, K. M. Butt, K. L. Wong, K. W. Chan, W. Lim, K. F. Shortridge, K. Y. Yuen, J. S. M. Peiris, and L. L. M. Poon. 2003. Isolation and characterization of viruses related to the SARS coronavirus from animals in Southern China. Science. 302:276-278.

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Footnote 5

Zhong, N. S., B. J. Zheng, Y. M. Li, L. L. M. Poon, Z. H. Xie, K. H. Chan, P. H. Li, S. Y. Tan, Q. Chang, J. P. Xie, X. Q. Liu, J. Xu, D. X. Li, K. Y. Yuen, J. S. M. Peiris, and Y. Guan. 2003. Epidemiology and cause of severe acute respiratory syndrome (SARS) in Guangdong, People's Republic of China, in February, 2003. Lancet. 362:1353-1358.

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Footnote 6

Berger, A., C. Drosten, H. Doerr, M. Stürmer, and W. Preiser. 2004. Severe acute respiratory syndrome (SARS)—paradigm of an emerging viral infection. Journal of Clinical Virology. 29:13-22.

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Footnote 7

Peiris, J. S. M., S. T. Lai, L. L. M. Poon, Y. Guan, L. Y. C. Yam, W. Lim, J. Nicholls, W. K. S. Yee, W. W. Yan, M. T. Cheung, V. C. C. Cheng, K. H. Chan, D. N. C. Tsang, R. W. H. Yung, T. K. Ng, and K. Y. Yuen. 2003. Coronavirus as a possible cause of severe acute respiratory syndrome. Lancet. 361:1319-1325.

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Footnote 8

Drosten, C., S. Günther, W. Preiser, S. Van der Werf, H. -. Brodt, S. Becker, H. Rabenau, M. Panning, L. Kolesnikova, R. A. M. Fouchier, A. Berger, A. -. Burguière, J. Cinatl, M. Eickmann, N. Escriou, K. Grywna, S. Kramme, J. -. Manuguerra, S. Müller, V. Rickerts, M. Stürmer, S. Vieth, H. -. Klenk, A. D. M. E. Osterhaus, H. Schmitz, and H. W. Doerr. 2003. Identification of a novel coronavirus in patients with severe acute respiratory syndrome. N. Engl. J. Med. 348:1967-1976.

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Footnote 9

Rota, P. A., M. S. Oberste, S. S. Monroe, W. A. Nix, R. Campagnoli, J. P. Icenogle, S. Peñaranda, B. Bankamp, K. Maher, M. -. Chen, S. Tong, A. Tamin, L. Lowe, M. Frace, J. L. DeRisi, Q. Chen, D. Wang, D. D. Erdman, T. C. T. Peret, C. Burns, T. G. Ksiazek, P. E. Rollin, A. Sanchez, S. Liffick, B. Holloway, J. Limor, K. McCaustland, M. Olsen-Rasmussen, R. Fouchier, S. Günther, A. D. H. E. Osterhaus, C. Drosten, M. A. Pallansch, L. J. Anderson, and W. J. Bellini. 2003. Characterization of a novel coronavirus associated with severe acute respiratory syndrome. Science. 300:1394-1399.

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Footnote 10

Seto, W., D. Tsang, R. Yung, T. Ching, T. Ng, M. Ho, L. Ho, J. Peiris, and Advisors of Expert SARS group of Hospital Authority. 2003. Effectiveness of precautions against droplets and contact in prevention of nosocomial transmission of severe acute respiratory syndrome (SARS). The Lancet. 361:1519-1520.

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Footnote 11

Marra, M. A., S. J. M. Jones, C. R. Astell, R. A. Holt, A. Brooks-Wilson, Y. S. N. Butterfield, J. Khattra, J. K. Asano, S. A. Barber, S. Y. Chan, A. Cloutier, S. M. Coughlin, D. Freeman, N. Girn, O. L. Griffith, S. R. Leach, M. Mayo, H. McDonald, S. B. Montgomery, P. K. Pandoh, A. S. Petrescu, A. G. Robertson, J. E. Schein, A. Siddiqui, D. E. Smailus, J. M. Stott, G. S. Yang, F. Plummer, A. Andonov, H. Artsob, N. Bastien, K. Bernard, T. F. Booth, D. Bowness, M. Czub, M. Drebot, L. Fernando, R. Flick, M. Garbutt, M. Gray, A. Grolla, S. Jones, H. Feldmann, A. Meyers, A. Kabani, Y. Li, S. Normand, U. Stroher, G. A. Tipples, S. Tyler, R. Vogrig, D. Ward, B. Watson, R. C. Brunham, M. Krajden, M. Petric, D. M. Skowronski, C. Upton, and R. L. Roper. 2003. The genome sequence of the SARS-associated coronavirus. Science. 300:1399-1404.

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Footnote 12

Heymann, D. L. 2008. Control of Communicable Diseases Manual. American Public Health Association, Washington, D.C.

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Footnote 13

Peiris, J. S. M., C. M. Chu, V. C. C. Cheng, K. S. Chan, I. F. N. Hung, L. L. M. Poon, K. I. Law, B. S. F. Tang, T. Y. W. Hon, C. S. Chan, K. H. Chan, J. S. C. Ng, B. J. Zheng, W. L. Ng, R. W. M. Lai, Y. Guan, and K. Y. Yuen. 2003. Clinical progression and viral load in a community outbreak of coronavirus-associated SARS pneumonia: A prospective study. Lancet. 361:1767-1772.

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Footnote 14

Anonymous 2004. Summary of Probable SARS Cases with Onset of Illness from 1 November 2002 to 31 July 2003.

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Footnote 15

Anonymous 2003. Update 49 SARS case fatality ratio, incubation period, July 3rd 2003.

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Footnote 16

Encyclopedia Britannica, S. Pettygrove, and K. Rogers. March 15, 2016. Attack Rate: Epidemiology.

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Footnote 17

Goh, D. L., B. W. Lee, K. S. Chia, B. H. Heng, M. Chen, S. Ma, and C. C. Tan. 2004. Secondary household transmission of SARS, Singapore. Emerg. Infect. Dis. 10:232-234.

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Footnote 18

Hon, K. L. E., C. W. Leung, W. T. F. Cheng, P. K. S. Chan, W. C. W. Chu, Y. W. Kwan, A. M. Li, N. C. Fong, P. C. Ng, M. C. Chiu, C. K. Li, J. S. Tam, and T. F. Fok. 2003. Clinical presentations and outcome of severe acute respiratory syndrome in children. Lancet. 361:1701-1703.

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Footnote 19

Yudin, M. H., D. M. Steele, M. D. Sgro, S. E. Read, P. Kopplin, and K. A. Gough. 2005. Severe acute respiratory syndrome in pregnancy. Obstet. Gynecol. 105:124-127.

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Footnote 20

Wong, S., K. Chow, and M. Swiet. 2003. Severe acute respiratory syndrome and pregnancy. BJOG: An International Journal of Obstetrics & Gynaecology. 110:641-642.

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Footnote 21

Kuiken, T., R. A. Fouchier, M. Schutten, G. F. Rimmelzwaan, G. Van Amerongen, D. van Riel, J. D. Laman, T. de Jong, G. van Doornum, and W. Lim. 2003. Newly discovered coronavirus as the primary cause of severe acute respiratory syndrome. The Lancet. 362:263-270.

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Footnote 22

Subbarao, K., J. McAuliffe, L. Vogel, G. Fahle, S. Fischer, K. Tatti, M. Packard, W. J. Shieh, S. Zaki, and B. Murphy. 2004. Prior infection and passive transfer of neutralizing antibody prevent replication of severe acute respiratory syndrome coronavirus in the respiratory tract of mice. J. Virol. 78:3572-3577.

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Footnote 23

Channappanavar, R., and S. Perlman. 2017. Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology, p. 1-11. In Anonymous Seminars in Immunopathology. Springer.

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Footnote 24

Wu, D., C. Tu, C. Xin, H. Xuan, Q. Meng, Y. Liu, Y. Yu, Y. Guan, Y. Jiang, X. Yin, G. Crameri, M. Wang, C. Li, S. Liu, M. Liao, L. Feng, H. Xiang, J. Sun, J. Chen, Y. Sun, S. Gu, N. Liu, D. Fu, B. T. Eaton, L. F. Wang, and X. Kong. 2005. Civets are equally susceptible to experimental infection by two different severe acute respiratory syndrome coronavirus isolates. J. Virol. 79:2620-2625.

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Footnote 25

Weingartl, H. M., J. Copps, M. A. Drebot, P. Marszal, G. Smith, J. Gren, M. Andova, J. Pasick, P. Kitching, and M. Czub. 2004. Susceptibility of pigs and chickens to SARS coronavirus. Emerg. Infect. Dis. 10:179-184.

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Footnote 26

Swayne, D. E., D. L. Suarez, E. Spackman, T. M. Tumpey, J. R. Beck, D. Erdman, P. E. Rollin, and T. G. Ksiazek. 2004. Domestic poultry and SARS coronavirus, southern China. Emerg. Infect. Dis. 10:914-916.

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Footnote 27

Wenzel, R. P., and M. B. Edmond. 2003. Listening to SARS: Lessons for Infection Control. Ann. Intern. Med. 139:592-593.

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Footnote 28

Lai, M. Y., P. K. Cheng, and W. W. Lim. 2005. Survival of severe acute respiratory syndrome coronavirus. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America. 41:e67-71.

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Footnote 29

Dwosh, H. A., H. H. Hong, D. Austgarden, S. Herman, and R. Schabas. 2003. Identification and containment of an outbreak of SARS in a community hospital. CMAJ. 168:1415-1420.

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Footnote 30

Li, W., S. K. Wong, F. Li, J. H. Kuhn, I. C. Huang, H. Choe, and M. Farzan. 2006. Animal origins of the severe acute respiratory syndrome coronavirus: insight from ACE2-S-protein interactions. J. Virol. 80:4211-4219.

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Footnote 31

Ksiazek, T. G., D. Erdman, C. S. Goldsmith, S. R. Zaki, T. Peret, S. Emery, S. Tong, C. Urbani, J. A. Comer, W. Lim, P. E. Rollin, S. F. Dowell, A. -. Ling, C. D. Humphrey, W. -. Shieh, J. Guarner, C. D. Paddock, P. Roca, B. Fields, J. DeRisi, J. -. Yang, N. Cox, J. M. Hughes, J. W. LeDuc, W. J. Bellini, and L. J. Anderson. 2003. A novel coronavirus associated with severe acute respiratory syndrome. N. Engl. J. Med. 348:1953-1966.

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Footnote 32

Zhao, Z., F. Zhang, M. Xu, K. Huang, W. Zhong, W. Cai, Z. Yin, S. Huang, Z. Deng, M. Wei, J. Xiong, and P. M. Hawkey. 2003. Description and clinical treatment of an early outbreak of severe acute respiratory syndrome (SARS) in Guangzhou, PR China. J. Med. Microbiol. 52:715-720.

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Footnote 33

Tu, C., G. Crameri, X. Kong, J. Chen, Y. Sun, M. Yu, H. Xiang, X. Xia, S. Liu, T. Ren, Y. Yu, B. T. Eaton, H. Xuan, and L. F. Wang. 2004. Antibodies to SARS coronavirus in civets. Emerg. Infect. Dis. 10:2244-2248.

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Footnote 34

Lim, P. L., A. Kurup, G. Gopalakrishna, K. P. Chan, C. W. Wong, L. C. Ng, S. Y. Se-Thoe, L. Oon, X. Bai, L. W. Stanton, Y. Ruan, L. D. Miller, V. B. Vega, L. James, P. L. Ooi, C. S. Kai, S. J. Olsen, B. Ang, and Y. -. Leo. 2004. Laboratory-Acquired Severe Acute Respiratory Syndrome. N. Engl. J. Med. 350:1740-1745.

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Footnote 35

Orellana, C. 2004. Laboratory-acquired SARS raises worries on biosafety. The Lancet Infectious Diseases. 4:64.

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Footnote 36

Normile, D. 2004. Mounting Lab Accidents Raise SARS Fears. Science. 304:659-661.

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Footnote 37

Liang, G., Q. Chen, J. Xu, Y. Liu, W. Lim, J. S. M. Peiris, L. J. Anderson, L. Ruan, H. Li, B. Kan, B. Di, P. Cheng, K. H. Chan, D. D. Erdman, S. Gu, X. Yan, W. Liang, D. Zhou, L. Haynes, S. Duan, X. Zhang, H. Zheng, Y. Gao, S. Tong, D. Li, L. Fang, P. Qin, W. Xu, J. Huang, Z. Wan, K. Zheng, J. Li, X. Deng, L. Diao, H. Zhou, P. Huang, W. Zhang, H. Zheng, H. Zhong, S. Xie, W. Li, J. Wang, Y. Zhong, J. Lin, M. Yan, H. Wang, W. Li, E. Zhang, Q. Hao, X. Dong, H. Wang, W. Zhou, L. Zhang, W. Wang, Y. Zhuang, J. Yu, Q. Zhang, Z. Zhu, Y. Zhang, M. Lai, P. Choy, L. L. M. Poon, Y. Guan, T. Peret, K. Felton, S. Emery, S. Chern, B. Cook, X. Lu, A. Tamin, C. Miao, and M. Dillon. 2004. Laboratory diagnosis of four recent sporadic cases of community-acquired SARS, Guangdong Province, China. Emerging Infectious Diseases. 10:1774-1781.

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Wang, L. -., Z. Shi, S. Zhang, H. Field, P. Daszak, and B. T. Eaton. 2006. Review of bats and SARS. Emerging Infectious Diseases. 12:1834-1840.

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Footnote 39

Donaldson, E. F., A. N. Haskew, J. E. Gates, J. Huynh, C. J. Moore, and M. B. Frieman. 2010. Metagenomic Analysis of the Virome of three North American Bat Species: Viral Diversity Between Different Bat Species that Share a Common Habitat. J. Virol. 84: 13004-13018.

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Footnote 40

Gralinski, L. E., A. Bankhead 3rd, S. Jeng, V. D. Menachery, S. Proll, S. E. Belisle, M. Matzke, B. J. Webb-Robertson, M. L. Luna, A. K. Shukla, M. T. Ferris, M. Bolles, J. Chang, L. Aicher, K. M. Waters, R. D. Smith, T. O. Metz, G. L. Law, M. G. Katze, S. McWeeney, and R. S. Baric. 2013. Mechanisms of severe acute respiratory syndrome coronavirus-induced acute lung injury. MBio. 4:10.1128/mBio.00271-13.

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Footnote 41

Rockx, B., T. Sheahan, E. Donaldson, J. Harkema, A. Sims, M. Heise, R. Pickles, M. Cameron, D. Kelvin, and R. Baric. 2007. Synthetic reconstruction of zoonotic and early human severe acute respiratory syndrome coronavirus isolates that produce fatal disease in aged mice. J. Virol. 81:7410-7423.

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Footnote 42

Rockx, B., F. Feldmann, D. Brining, D. Gardner, R. LaCasse, L. Kercher, D. Long, R. Rosenke, K. Virtaneva, and D. E. Sturdevant. 2011. Comparative pathogenesis of three human and zoonotic SARS-CoV strains in cynomolgus macaques. PloS One. 6:e18558.

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Footnote 43

Ng, O., and Y. Tan. 2017. Understanding bat SARS-like coronaviruses for the preparation of future coronavirus outbreaks—Implications for coronavirus vaccine development. Human Vaccines & Immunotherapeutics. 13:186-189.

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Footnote 44

Li, W., Z. Shi, M. Yu, W. Ren, C. Smith, J. H. Epstein, H. Wang, G. Crameri, Z. Hu, H. Zhang, J. Zhang, J. McEachern, H. Field, P. Daszak, B. T. Eaton, S. Zhang, and L. -. Wang. 2005. Bats are natural reservoirs of SARS-like coronaviruses. Science. 310:676-679.

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Footnote 45

Lau, S. K. P., P. C. Y. Woo, K. S. M. Li, Y. Huang, H. -. Tsoi, B. H. L. Wong, S. S. Y. Wong, S. -. Leung, K. -. Chan, and K. -. Yuen. 2005. Severe acute respiratory syndrome coronavirus-like virus in Chinese horseshoe bats. Proc. Natl. Acad. Sci. U. S. A. 102:14040-14045.

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Footnote 46

Rihtaric, D., P. Hostnik, A. Steyer, J. Grom, and I. Toplak. 2010. Identification of SARS-like coronaviruses in horseshoe bats (Rhinolophus hipposideros) in Slovenia. Arch. Virol. 155:507-514.

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Footnote 47

Hou, Y., C. Peng, M. Yu, Y. Li, Z. Han, F. Li, L. F. Wang, and Z. Shi. 2010. Angiotensin-converting enzyme 2 (ACE2) proteins of different bat species confer variable susceptibility to SARS-CoV entry. Arch. Virol. 155:1563-1569.

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Rabenau, H. F., J. Cinatl, B. Morgenstern, G. Bauer, W. Preiser, and H. W. Doerr. 2005. Stability and inactivation of SARS coronavirus. Med. Microbiol. Immunol. (Berl. ). 194:1-6.

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Duan, S. -., X. -. Zhao, R. -. Wen, J. -. Huang, G. -. Pi, S. -. Zhang, J. Han, S. -. Bi, L. Ruan, and X. -. Dong. 2003. Stability of SARS Coronavirus in Human Specimens and Environment and Its Sensitivity to Heating and UV Irradiation. Biomedical and Environmental Sciences. 16:246-255.

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Bonny, T. S., S. Yezli, and J. A. Lednicky. 2017. Isolation and identification of human coronavirus 229E from frequently touched environmental surfaces of a university classroom that is cleaned daily. Am. J. Infect. Control. 46:105-107.

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Jernigan, J. A., D. E. Low, and R. F. Helfand. 2004. Combining Clinical and Epidemiologic Features for Early Recognition of SARS. Emerging Infectious Diseases. 10:327-333.

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Footnote 53

Stockman, L. J., R. Bellamy, and P. Garner. 2006. SARS: Systematic review of treatment effects. PLoS Medicine. 3:1525-1531.

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Footnote 54

Jiang, S., Y. He, and S. Liu. 2005. SARS vaccine development. Emerg. Infect. Dis. 11:1016-1020.

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Footnote 55

See, R. H., A. N. Zakhartchouk, M. Petric, D. J. Lawrence, C. P. Mok, R. J. Hogan, T. Rowe, L. A. Zitzow, K. P. Karunakaran, and M. M. Hitt. 2006. Comparative evaluation of two severe acute respiratory syndrome (SARS) vaccine candidates in mice challenged with SARS coronavirus. J. Gen. Virol. 87:641-650.

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Footnote 56

Roper, R. L., and K. E. Rehm. 2009. SARS vaccines: where are we? Expert Review of Vaccines. 8:887-898.

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Footnote 57

Sheahan, T. P., A. C. Sims, R. L. Graham, V. D. Menachery, L. E. Gralinski, J. B. Case, S. R. Leist, K. Pyrc, J. Y. Feng, I. Trantcheva, R. Bannister, Y. Park, D. Babusis, M. O. Clarke, R. L. Mackman, J. E. Spahn, C. A. Palmiotti, D. Siegel, A. S. Ray, T. Cihlar, R. Jordan, M. R. Denison, and R. S. Baric. 2017. Broad-spectrum antiviral GS-5734 inhibits both epidemic and zoonotic coronaviruses. Sci. Transl. Med. 9.

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Footnote 58

Pathogens, H., and T. Act. 2009. SC 2009, c. 24. Government of Canada. Second Session, Fortieth Parliament. 57-58.

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Footnote 59

Public Health Agency of Canada. 2015. Canadian Biosafety Standard. Government of Canada, Ottawa.

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