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      Rapid response research to emerging infectious diseases: lessons from SARS

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          Abstract

          New and emerging infectious diseases continue to plague the world, and there is significant concern that recombinant infectious agents can be used as bioterrorism threats. Microbiologists are increasingly being asked to apply their scientific knowledge to respond to these threats. The recent pandemic caused by the severe acute respiratory syndrome (SARS) coronavirus illustrated not only how a newly evolved pathogen can rapidly spread throughout the world but also how the global community can unite to identify the causative agent and control its spread. Rapid response research mechanisms, such as those used by the SARS Accelerated Vaccine Initiative (SAVI), have shown that the application of emergency management techniques, together with rapid response research, can be highly effective when applied appropriately to new infectious diseases.

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          Characterization of a novel coronavirus associated with severe acute respiratory syndrome.

          P Rota (2003)
          In March 2003, a novel coronavirus (SARS-CoV) was discovered in association with cases of severe acute respiratory syndrome (SARS). The sequence of the complete genome of SARS-CoV was determined, and the initial characterization of the viral genome is presented in this report. The genome of SARS-CoV is 29,727 nucleotides in length and has 11 open reading frames, and its genome organization is similar to that of other coronaviruses. Phylogenetic analyses and sequence comparisons showed that SARS-CoV is not closely related to any of the previously characterized coronaviruses.
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            Identification of severe acute respiratory syndrome in Canada.

            Susan M Poutanen, Donald Low, Bonnie Henry … (2003)
            Severe acute respiratory syndrome (SARS) is a condition of unknown cause that has recently been recognized in patients in Asia, North America, and Europe. This report summarizes the initial epidemiologic findings, clinical description, and diagnostic findings that followed the identification of SARS in Canada. SARS was first identified in Canada in early March 2003. We collected epidemiologic, clinical, and diagnostic data from each of the first 10 cases prospectively as they were identified. Specimens from all cases were sent to local, provincial, national, and international laboratories for studies to identify an etiologic agent. The patients ranged from 24 to 78 years old; 60 percent were men. Transmission occurred only after close contact. The most common presenting symptoms were fever (in 100 percent of cases) and malaise (in 70 percent), followed by nonproductive cough (in 100 percent) and dyspnea (in 80 percent) associated with infiltrates on chest radiography (in 100 percent). Lymphopenia (in 89 percent of those for whom data were available), elevated lactate dehydrogenase levels (in 80 percent), elevated aspartate aminotransferase levels (in 78 percent), and elevated creatinine kinase levels (in 56 percent) were common. Empirical therapy most commonly included antibiotics, oseltamivir, and intravenous ribavirin. Mechanical ventilation was required in five patients. Three patients died, and five have had clinical improvement. The results of laboratory investigations were negative or not clinically significant except for the amplification of human metapneumovirus from respiratory specimens from five of nine patients and the isolation and amplification of a novel coronavirus from five of nine patients. In four cases both pathogens were isolated. SARS is a condition associated with substantial morbidity and mortality. It appears to be of viral origin, with patterns suggesting droplet or contact transmission. The role of human metapneumovirus, a novel coronavirus, or both requires further investigation. Copyright 2003 Massachusetts Medical Society
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              Comparative full-length genome sequence analysis of 14 SARS coronavirus isolates and common mutations associated with putative origins of infection

              Yijun Ruan, Chia Wei, Ai Ling … (2003)
              Summary Background The cause of severe acute respiratory syndrome (SARS) has been identified as a new coronavirus. Whole genome sequence analysis of various isolates might provide an indication of potential strain differences of this new virus. Moreover, mutation analysis will help to develop effective vaccines. Methods We sequenced the entire SARS viral genome of cultured isolates from the index case (SIN2500) presenting in Singapore, from three primary contacts (SIN2774, SIN2748, and SIN2677), and one secondary contact (SIN2679). These sequences were compared with the isolates from Canada (TOR2), Hong Kong (CUHK-W1 and HKU39849), Hanoi (URBANI), Guangzhou (GZ01), and Beijing (BJ01, BJ02, BJ03, BJ04). Findings We identified 129 sequence variations among the 14 isolates, with 16 recurrent variant sequences. Common variant sequences at four loci define two distinct genotypes of the SARS virus. One genotype was linked with infections originating in Hotel M in Hong Kong, the second contained isolates from Hong Kong, Guangzhou, and Beijing with no association with Hotel M (p<0.0001). Moreover, other common sequence variants further distinguished the geographical origins of the isolates, especially between Singapore and Beijing. Interpretation Despite the recent onset of the SARS epidemic, genetic signatures are emerging that partition the worldwide SARS viral isolates into groups on the basis of contact source history and geography. These signatures can be used to trace sources of infection. In addition, a common variant associated with a non-conservative aminoacid change in the S1 region of the spike protein, suggests that immunological pressures might be starting to influence the evolution of the SARS virus in human populations. Published online May 9, 2003 http://image.thelancet.com/extras/03art4454web.pdf
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                Author and article information

                Contributors
                B. Brett Finlay: bfinlay@interchange.ubc.ca
                Bio :

                B. Brett Finlay is the Peter Wall and CIHR Distinguished Professor in the Biotechnology Laboratory at the University of British Columbia. He obtained a B.Sc. (Hons) and Ph.D. in Biochemistry at the University of Alberta. His postdoctoral studies were undertaken with Professor Stanley Falkow in the Department of Medical Microbiology and Immunology at Stanford University School of Medicine. His research interests include the interactions between pathogenic Escherichia coli and Salmonella spp. and host cells at a molecular level, as well as how these pathogens circumvent innate host responses. He has won several prestigious awards, including the E.W.R. Steacie Prize in 1999, the CSM Fisher Scientific Award, a CIHR Distinguished Investigator award and is a Fellow of the Royal Society of Canada.

                Raymond H. See:
                Bio :

                Raymond See received his Ph.D. from the University of British Columbia Department of Experimental Pathology in 1992 where he studied the mechanism of action of staphylococcal toxic shock syndrome toxin-1 on human peripheral blood mononuclear cells. During his Ph.D. training, he received numerous awards for his research, including the Western Society for Investigation Student Award and the Canadian Society for Clinical Investigation Trainee Award. From 1993 to 1999 he did his postdoctoral training at Harvard Medical School of Pathology in Boston and was supported by a Medical Research Council (now CIHR) postdoctoral fellowship award. During the course of his graduate and postdoctoral training, he has published 22 papers in peer-reviewed journals. After his postdoctoral training, he joined Consensus Pharmaceuticals Inc. (Medford, Massachusetts, USA) as a senior scientist. In 2000, he returned to Vancouver as a project leader for Xenon Genetics Inc. There, he led a team responsible for biological assay development as well as small-molecule screening for two major drug targets related to lipid metabolism. He joined SAVI as the programme director of vaccine development in November 2003.

                Robert C. Brunham:
                Bio :

                Robert C. Brunham is Director of the University of British Columbia Centre for Disease Control (UBC CDC) and Medical Director of the British Columbia Centre for Disease Control Society (BCCDC). He is a Professor in the Department of Medicine, Division of Infectious Diseases at the University of British Columbia. He obtained his M.D. from UBC in 1972 and completed training in Internal Medicine at McGill University in 1978. From 1978 to 1982, Professor Brunham was a Medical Research Council of Canada research fellow at the University of Washington, USA under the supervision of Dr King Holmes. From 1982 to 1999 he was at the University of Manitoba, Canada, where he was Professor and Chairman of the Department of Medical Microbiology and Infectious Diseases from 1988 to 1999. His research interests centre on the immunology, epidemiology and genomics of infectious diseases. He has published more than 200 articles and book chapters on various aspects of infectious diseases, with an emphasis on sexually transmitted diseases. Much of his work has dealt with the immunobiology and epidemiology of Chlamydia trachomatis with the goal of developing a vaccine. As Director of the UBC CDC, his recent work has dealt with emerging infectious diseases such as SARS.

                Journal
                Journal ID (nlm-ta): Nat Rev Microbiol
                Journal ID (iso-abbrev): Nat. Rev. Microbiol
                Title: Nature Reviews. Microbiology
                Publisher: Nature Publishing Group UK (London )
                ISSN (Print): 1740-1526
                ISSN (Electronic): 1740-1534
                Publication date (Print): 2004
                Volume: 2
                Issue: 7
                Pages: 602-607
                Affiliations
                [1 ]GRID grid.17091.3e, ISNI 0000 0001 2288 9830, Biotechnology Laboratory and Departments of Biochemistry and Molecular Biology and Microbiology and Immunology, , University of British Columbia, ; Vancouver, V6T 1Z3 British Columbia Canada
                [2 ]GRID grid.17091.3e, ISNI 0000 0001 2288 9830, Department of Medicine, Division of Infectious Diseases, , BC CDC, University of British Columbia, ; Vancouver, V6T 1Z3 British Columbia Canada
                Article
                Publisher ID: BFnrmicro930
                DOI: 10.1038/nrmicro930
                PMC ID: 7097457
                PubMed ID: 15197395
                SO-VID: 9849a57c-0327-413d-940e-82231a1993be
                Copyright © © Nature Publishing Group 2004
                License:

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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