SARS Virus

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  Agents of Bioterrorism

  Pathogens and Their Weaponization

  • Geoffrey Zubay(Author)
  • 2008(Publication Date)
  • Columbia University Press

    (Publisher)

  CHAPTER 9 SEVERE ACUTE RESPIRATORY SYNDROME (SARS) Joseph Patrick Ward and Maria E. Garrido A s of early 2003, people thought that a new virus spreading throughout the world faster than the Internet could happen only in bad dreams or modern science-fiction movies. Then we learned about SARS-CoV, the virus that causes severe acute respiratory syndrome (SARS). Less than 7 months after it was first reported, SARS had taken the lives of approximately 800 people and infected a total of more than 8400 people worldwide. SARS-CoV belongs to the family of coronaviruses. The coronaviruses (order Nidovirales, family Coronaviridae, genus Coronavirus) are members of a family of large, enveloped, positive-sense, single-stranded RNA viruses that replicate in the cytoplasm of host cells. Coronaviruses are highly species-specific, and the family had only included two human-infecting viruses prior to the discovery of SARS-CoV. Coronaviruses are divided into three groups, and exactly where SARS-CoV fits into the three groups has been debated. It has even been suggested that SARS-CoV represents a new, fourth group of coronaviruses. No vaccine or effective treatment currently exists for SARS. 11 The natural host has not yet been identified despite widespread speculation that the host is the civet, a cat-like mammal from which a virus similar to SARS-CoV has been isolated. Because of the circumstances surrounding the SARS outbreak of 2003 and the very small number of cases that have been reported since, it has been proposed that the 2003 outbreak was strictly a one-time event. Although much research was conducted during and immediately after the 2003 outbreak, little research has been done on the disease and its causative agent in the latter half of 2004

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  Severe Acute Respiratory Syndrome (Sars): From Benchtop To Bedside

  From Benchtop to Bedside

  • Joseph Jao Yiu Sung(Author)
  • 2004(Publication Date)
  • World Scientific

    (Publisher)

  3 Virology of SARS Paul KS Chan On 16 April 2003, the World Health Organization (WHO) announced that a novel coronavirus is the cause of the global outbreak of severe acute res-piratory syndrome (SARS). The success and speed in identification of the culprit is a result of an unprecedented international collaboration involv-ing 13 virus laboratories from 10 countries. 1,2 WHO and the network of laboratories have decided to dedicate their detection and characterization of the culprit virus to Dr. Carlo Urbani, who was the first WHO officer to detect the outbreak in Vietnam and later died of the infection. 3,4 In 1882, Heinrich Koch, a German bacteriologist, set out four postu-lates for proving the etiological association between an infectious disease and its causative agent. This novel coronavirus fulfils these gold standard criteria. Firstly, the organism must be found in all cases. It has been shown that all SARS cases had serological evidence of infection with the novel coronavirus. 5–7 Secondly, it must be isolated from the host and grown in pure culture. The novel coronavirus has been isolated from post-mortem lung tissues of fatal SARS cases, and pure culture was grown from monkey kidney cells. 5–7 The third and fourth postulates require the reproduction of the original disease when the organism is 21 introduced to a susceptible host, and it must be found in the experimental infected host. Cynomolgus macaques (Macaca fascicularis) inoculated with the novel coronavirus, isolated from a fatal SARS case, developed lung pathologies indistinguishable from those observed in fatal human SARS cases. The infected macaques showed seroconversion, and it was possible to isolate the viruses from nasal and throat secretions, and stool samples. 8,9 With these evidences, it is appropriate to refer to the novel coronavirus as SARS-associated coronavirus (SARS-CoV). CORONAVIRUS Coronavirus is a group of common pathogens that infects a variety of mammals and birds worldwide.

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  Emerging Viruses in Human Populations

  • Edward Tabor(Author)
  • 2006(Publication Date)
  • Elsevier Science

    (Publisher)

  Emerging Viruses in Human Populations Edward Tabor (Editor) r 2007 Elsevier B.V. All rights reserved DOI 10.1016/S0168-7069(06)16004-8 43 Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) Tommy R. Tong Department of Pathology, Princess Margaret Hospital, Laichikok, Kowloon, Hong Kong, China Severe acute respiratory syndrome (SARS) caused by a coronavirus (CoV), SARS-CoV, emerged into human populations in south China ( Anon., 2003d ; Peiris et al., 2003b,c ; Poon et al., 2004a ) from bats ( Guan et al., 2003 ; Kan et al., 2005 ; Lau et al., 2005 ; Li et al., 2005d ; Normile, 2005 ) in late 2002. Subsequently, SARS-CoV that had adapted to humans caused an epidemic in 29 countries and regions to which it had been carried by airline passengers. The epidemic was controlled by public health measures coordinated by the WHO and on July 5, 2003 it was of-ficially declared to have ended. Because of these public health measures, a pan-demic was averted ( Enserink, 2003b ). Close to 10% of the 8000 persons infected in this epidemic died. Molecular studies dissected the adaptation of this virus as it jumped from an intermediary animal, the civet, to humans, giving us valuable insights into processes of molecular emergence. Global research efforts are con-tinuing to increase our understanding of the virus, the pathogenesis of the disease it causes (SARS), the ‘‘heterogeneity of individual infectiousness’’ (described below) as well as shedding light on how to prepare for other emerging viral diseases. Promising drugs and vaccines have been identified. The milestones achieved have resulted from a truly international effort. The beginning of the epidemic and the identification of SARS-CoV The epidemic began in Guangdong province, China, in late 2002. It spread to Hong Kong on February 21, 2003, and from there to other parts of the world.

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  Manual of Security Sensitive Microbes and Toxins

  • Dongyou Liu(Author)
  • 2014(Publication Date)
  • CRC Press

    (Publisher)

  215 19 19.1 INTRODUCTION Severe acute respiratory syndrome coronavirus (SARS CoV) emerged in 2003 as a global health threat that causes a life-threatening infectious respiratory disease. The first SARS out-break occurred in November 2002 in Guangdong Province, China, and the epidemic quickly spread to more than 30 coun-tries. There were more than 8000 cases and approximately 800 deaths during the outbreak in 2002–2003. 1 Fortunately, the outbreak triggered a successful global response, and the spread of the disease was stopped at the end of June 2003 and did not reach the scale of an influenza pandemic. Before the appearance of SARS CoV, human coronaviruses, such as 229E and OC43, were relatively obscure and usually associ-ated with a mild upper respiratory tract infection presenting symptoms of the common cold. In contrast, animal coronavi-ruses are responsible for a variety of severe diseases in domes-ticated animals. 2–8 The severity and sudden onset of symptoms of atypical pneumonia with dry cough and persistent high fever, which is drastically different from symptoms of the pre-viously known human pathogenic coronaviruses, suggested that SARS CoV emerged through interspecies transmission. 1 After the outbreak, the origin of the SARS CoV was traced back to exotic animals, such as the Himalayan palm civets ( Paguma larvata ) and raccoon dogs ( Nyctereutes procyonoides ), sold in Chinese wet markets. 9 Subsequent studies found the presence of SARS CoV in various ani-mals including Chinese ferret-badger ( Melogale moschata ) and several bat species. Furthermore, these studies also sug-gested that although P. larvata may have been the source of animal-to-human interspecies transmission that precipitated the SARS outbreak, these animals only serve as intermedi-ate hosts while bats, Chinese horseshoe bats ( Rhinolophus sinicus ) in particular, are the likely animal reservoir of SARS CoV.

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  Genetics and Evolution of Infectious Diseases

  • Michel Tibayrenc(Author)
  • 2010(Publication Date)
  • Elsevier

    (Publisher)

  27. Evolution of SARS Coronavirus and the Relevance of Modern Molecular Epidemiology

  Zhengli Shi1 * and Lin-Fa Wang2

  1 State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences (CAS), Wuhan, China

  2 CSIRO Livestock Industries, Australian Animal Health Laboratory, Geelong, Australia

  * E-mail: [email protected]

  Severe acute respiratory syndrome (SARS) is the first major zoonotic infectious disease of the twenty-first century. The disease, originally termed “atypical pneumonia,” was first recognized in November 2002 in Guangdong Province, China, which spread rapidly to 26 countries within 5 months and eventually led to 8096 human infection cases and 774 deaths. A previously unrecognized coronavirus, SARS coronavirus (SARS-CoV), was later identified as the causative agent of the SARS. Subsequent investigation indicated that the source of the human infections was most likely originated from infected wildlife animals traded in the live animal markets, with masked palm civets being considered the most prominent and important carrier. Large-scale culling of civets appeared to have prevented further outbreaks in the region. Further epidemiological studies showed that civets are intermediate hosts of SARS-CoV, and bats are the likely natural reservoir of SARS-CoV and a large number of SARS-like coronaviruses (SL-CoVs). Detailed analysis of the massive SARS-CoV genomic sequence data accumulated indicated that SARS-CoV experienced a strong selection pressure during different outbreak phases in humans as well as interspecies transmission from animals to humans. The spike glycoprotein (S) of SARS-CoV plays a key role in virus–host interaction and hence is a key determinant of interspecies transmission. It has been shown that minor changes of amino acid (aa) residues in the S protein could lead to dramatic changes in virus susceptibility in animal and human hosts. This chapter will focus on the genetics and evolution of SARS-CoVs and SL-CoVs in humans, civets, and bats. The events of SARS outbreaks and the accompanying response activities highlight the importance of modern molecular epidemiology in disease investigation and the urgent need to broaden the screening and investigation of unknown viruses in wildlife animals.

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  Emerging Viral Diseases of Southeast Asia

  • S. K. Lal, B. W. J. Mahy(Authors)
  • 2006(Publication Date)
  • S. Karger

    (Publisher)

  By March 2003, the disease had spread to Hong Kong, Vietnam, Taiwan, Singapore and Canada. In response to this global threat, the WHO provided a preliminary case definition and initiated a world-wide network of laboratories to investigate the cause of what is now called severe acute respiratory syndrome (SARS) [1, 2]. Singapore General Hospital (SGH) formed an integral part of the WHO network of laboratories, providing a vital up-to-date information resource for researchers in Singapore, as well as making viral samples available for research purposes internationally. Fielding/Tan 2 The causative agent of SARS was identified as a novel coronavirus, now known as coronavirus (SARS-CoV) (for reviews, see [3–6]). SARS eventually spread to about 30 countries on 5 continents, infecting more than 8,000 people and resulting in 774 deaths. Since SARS had a dramatic impact on the health system and economy of Singapore, researchers of the island-nation became involved in the fight against this deadly disease early on. Subsequently, the con-tribution of research from Singapore to understanding this potentially lethal infection and its causative agent has been significant. This review aims to record the contributions made by researchers in Singapore to the current under-standing of SARS, including the epidemiology in the Singapore setting. Also the development of diagnostic tests will be discussed. Finally, a summary of the research of the proteins associated with the SARS-CoV genome will be given. Epidemiology Singapore By mid-March 2003, SARS reached Singapore and was subsequently traced to three travelers returning from a holiday in Hong Kong [7, 8]. The index patient, a 23-year-old woman was admitted to Tan Tock Seng Hospital, Singapore, on March 1 with fever and a dry cough. Over the course of a few days, the virus spread rapidly from this patient to medical staff, patients and visi-tors, infecting 20 people in total, thereby initiating the SARS outbreak in Singapore [9].

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  New Generation Vaccines

  • Myrone M. Levine, Myron M. Levine, Gordon Dougan, Michael F. Good, Margaret A. Liu, Gary J. Nabel, James P. Nataro, Rino Rappuoli, Myrone M. Levine, Myron M. Levine, Gordon Dougan, Michael F. Good, Gary J. Nabel, James P. Nataro, Rino Rappuoli, Myrone M. Levine, Myron M. Levine, Gordon Dougan, Michael F. Good, Gary J. Nabel, James P. Nataro, Rino Rappuoli(Authors)
  • 2016(Publication Date)
  • CRC Press

    (Publisher)

  84 SARS Vaccines Kanta Subbarao Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, U.S.A. INTRODUCTION In February 2003, physicians at a hospital in Hanoi, Vietnam, sought advice from the local WHO office regarding a patient who had presented with an unusual influenza-like illness (1). Dr Carlo Urbani, an infectious disease specialist who responded to the request soon notified the WHO of an outbreak of severe respiratory disease. In the ensuing weeks, it became clear that similar outbreaks were occurring in several locations including Hong Kong, southern China, and Canada, and that patients in diverse locations had stayed at the same hotel in Hong Kong. The syndrome was called severe acute respiratory syndrome (SARS) and was characterized by fever, chills or rigors, headache, and nonspecific symptoms such as malaise and myalgias, followed by cough and dyspnea (2,3). Respiratory tract disease progressed to acute respiratory distress syndrome requiring intensive care and mechanical ventilation in more than 20% of patients. Prolonged hospitalizations associated with complications were reported, and advanced age was an inde-pendent correlate of adverse clinical outcome and increased mortality. The outbreak was notable for spread in health care settings, affecting large numbers of health care workers, and for a rapid dissemination to distant parts of the world by infected travelers. SARS first emerged in Guangdong province, China, around November 2002, where many of the affected individu-als had contact with the live game trade (3). By the time the outbreak was over in July 2003, the WHO recorded more than 8000 cases including 774 deaths.

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  Internet Discourse and Health Debates

  • K. Richardson(Author)
  • 2004(Publication Date)
  • Palgrave Macmillan

    (Publisher)

  5 SARS 90 SARS stands for Severe Acute Respiratory Syndrome, the new infectious disease which began in China in the second half of 2002 and was intro- duced to the world in March 2003. SARS as an ‘issue’ is different from mobile phones and cancer. Where the mobile phone debate begins with the ‘cause’ and reasons or speculates about effects, the discussion of SARS begins at the other end, with illness and death, and tries to work backwards to the probable causes of infection in particular cases. But there is similarity too. In both cases public interest in the topic has for many people a personal character. People are anxious to know if their normal behaviour – which might include travelling on a plane as well as using a cellphone – is going to put them on a danger list. In one case the risk is open – the danger might be cancer, or something else, or nothing at all – in the other case, it has a name – SARS – and a list of bodily symptoms. This chapter begins with a brief account of how the world learned about SARS in 2003. It is followed by a discussion of the role of the internet – websites and Usenet groups – in disseminating information and opinion with respect to this new disease on a global scale. My discussion of websites compares the online voice of global author- ity – that of the World Health Organization – with two other web con- tributions to the story of SARS. These are two very different ‘blogs’ – ‘SARS Watch’, a news digest, and ‘Wangjianshuo’s blog’, a diary-style account of one man’s life and thoughts within a Chinese city affected by SARS. In relation to newsgroups, the chapter focuses upon the three-and-a- half months following the crisis announcement. This is in contrast to the ten years of Usenet activity which were reviewed in the mobile tele- phone chapter. If the mobile phone issue is chronic, then the SARS issue K. Richardson, Internet Discourse and Health Debates © Kay Richardson 2005

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  Severe Acute Respiratory Syndrome

  • Malik Peiris, Larry J. Anderson, Albert D. M. E. Osterhaus, Klaus Stohr, Kwok-yung Yuen, Malik Peiris, Larry J. Anderson, Albert D. M. E. Osterhaus, Klaus Stohr, Kwok-yung Yuen(Authors)
  • 2008(Publication Date)
  • Wiley-Blackwell

    (Publisher)

  Research efforts need to concentrate on identifying the SARS CoV reservoir and understanding its ecology better. References 1 Haydon DT, Cleaveland S, Taylor LH et al . Iden-tifying reservoirs of infection: a conceptual and practical challenge. Emerg Infect Dis 2002; 8 : 1468–73. 2 Xu RH, He JF, Evans MR et al . Epidemiologic clues to SARS origin in China. Emerg Infect Dis 2004; 10 : 1030–7. 3 Zhong NS, Zheng BJ, Li YM et al. Epidemiology and cause of severe acute respiratory syndrome (SARS) in Guangdong, People’s Republic of China, in February 2003. Lancet 2003; 362 : 1355–8. 4 Guan Y, Zheng BJ, He YQ et al. Isolation and characterization of viruses related to SARS coro-navirus from animals in southern China. Science 2003; 302 : 276–8. CoV can cause potentially fatal disease in humans as previously recognized for ani-mal CoVs (Table 12.1). Because pneumonia and diarrhoea occur in SARS patients, this review will focus on animal CoVs that cause respiratory or respiratory/enteric disease (Table 12.1) because these may provide an insight into the pathogenesis and evolution of SARS. Coronavirus evolution and pathogenesis Group 1 porcine CoVs: models for enteric or respiratory CoV disease New strains with altered tissue tropism can arise from existing strains through muta-tion. For example, the porcine respiratory coronavirus (PRCV) is a less virulent variant of TGEV and feline infectious peritonitis virus (FIPV) is the virulent variant of feline enteric coronavirus (FECoV). 5,6 Alterna-tively, new strains may occur after recombi-nation events such as the potential S gene recombinants between canine coronavirus (CCoV) and FECoV type 1 leading to a new FECoV serotype (type 2) 6,7 or the acquisi-tion of an influenza group C-like haemag-glutinin (HE) by BCoV or its CoV ancestor. 8 In addition, like SARS, new animal strains have emerged from unknown sources such as the porcine epidemic diarrhoea virus (PEDV) that first appeared in Europe and Asia between 1978 and the 1980s.

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  Coronavirus Disease 2019 (Covid-19)

  A Clinical Guide

  • Ali Gholamrezanezhad, Michael P. Dube(Authors)
  • 2022(Publication Date)
  • Wiley-Blackwell

    (Publisher)

  (2021). Characteristics of SARS-CoV-2 and COVID-19. Nat. Rev. Microbiol. 19 (3): 141–154. 5 Mittal, A., Manjunath, K., Ranjan, R.K. et al. (2020). COVID-19 pandemic: insights into structure, function, and hACE2 receptor recognition by SARS-CoV-2. PLoS Pathog. 16 (8): e1008762. 6 World Health Organization (2021). WHO-convened global study of origins of SARS-CoV-2: China part. World Health Organization. https://www.who.int/ publications/i/item/ who-convened-global-study-of-origins-of-sars-cov-2- china-part. 7 Deng, S.-Q. and Peng, H.-J. (2020). Characteristics of and public health responses to the coronavirus disease 2019 outbreak in China. J. Clin. Med. 9 (2): 575. 8 Coronaviridae Study Group of the International Committee on Taxonomy of Viruses (2020). The species severe acute respiratory syndrome-related coronavirus: classifying 2019-nCoV and naming it SARS-CoV-2. Nat. Microbiol. 5 (4): 536. 9 Smithgall, M.C., Dowlatshahi, M., Spitalnik, S.L. et al. (2020). Types of assays for SARS-CoV-2 testing: a review. Lab. Med. 51 (5): e59–e65. 10 Schoeman, D. and Fielding, B.C. (2019). Coronavirus envelope protein: current knowledge. Virol. J. 16 (1): 69. 11 Netland, J., DeDiego, M.L., Zhao, J. et al. (2010). Immunization with an attenuated severe acute respiratory syndrome coronavirus deleted in E protein protects against lethal respiratory disease. Virology 399 (1): 120–128. 12 Almazán, F., DeDiego, M.L., Sola, I. et al. (2013). Engineering a replication-competent, propagation- defective Middle East respiratory syndrome coronavirus as a vaccine candidate. MBio 4 (5): e00650-13. 13 Zhou, P., Yang, X.L., Wang, X.G. et al. (2020). A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 579 (7798): 270–273. 14 Corti, D., Purcell, L.A., Snell, G., and Veesler, D. (2021). Tackling COVID-19 with neutralizing monoclonal antibodies. Cell 184 (12): 3086–3108. 15 Belouzard, S., Chu, V.C., and Whittaker, G.R.

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  Pathogenic Coronaviruses of Humans and Animals

  SARS, MERS, COVID-19, and Animal Coronaviruses with Zoonotic Potential

  • Lisa A. Beltz(Author)
  • 2022(Publication Date)
  • Academic Press

    (Publisher)

  Intervirol . 2016;59:163–169.

  86. Lee N, Hui D, Wu A, et al. Major outbreak of severe acute respiratory syndrome in Hong Kong . N Engl J Med . 2003;348(20):1986–1994.

  87. Booth SM, Matukas LM, Tomlinson GA, et al. Clinical features and short-term outcomes of 144 patients with SARS in the greater Toronto area . J Am Med Soc . 2003;289(21):2801–2809.

  88. Hung ECW, Chim SSC, Chan PKS, et al. Detection of SARS coronavirus RNA in the cerebrospinal fluid of a patient with severe acute respiratory syndrome . Clin Chem . 2003;49(12):2108–2109.

  89. Dube M, Le Coupanec A, Wong AHM, Rini JM, Desforges M, Talbot PJ. Axonal transport enables neuron-to-neuron propagation of human coronavirus . J Virol . 2018;92(17):e00404–18.

  90. Netland J, Meyerholz DK, Moore S, Cassell M, Perlman S. Severe acute respiratory syndrome coronavirus infection causes neuronal death in the absence of encephalitis in mice transgenic for human ACE2 . J Virol . 2008;82(15):7264–7275.

  91. Le Coupanec A, Desforges M, Meessen-Pinard M, et al. Cleavage of a neuroinvasive human respiratory virus spike glycoprotein by proprotein convertases modulates neurovirulence and virus spread within the central nervous system . PLoS Pathog . 2015;11:e1005261.

  92. Gu J, Gong E, Zhang B, et al. Multiple organ infection and the pathogenesis of SARS . J Exp Med . 2005;202(3):415–424.

  93. Xu J, Zhong S, Liu J, et al. Detection of severe acute respiratory syndrome coronavirus in the brain: potential role of the chemokine MIG in pathogenesis . Clin Infect Dis . 2005;41(8):1089–1096.

  94. Desforges M, Le Coupanec A, Dubeau P, et al. Human coronaviruses and other respiratory viruses: underestimated opportunistic pathogens of the central nervous system? . Viruses . 2019;12(1):14.

  95. Jacomy H, St-Jean JR, Brison E, Marceau G, Desforges M, Talbot PJ. Mutations in the spike glycoprotein of human coronavirus OC43 modulate disease in BALB/c mice from encephalitis to flaccid paralysis and demyelination . J Neurovirol

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