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      Possibility for reverse zoonotic transmission of SARS-CoV-2 to free-ranging wildlife: A case study of bats

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      1 , * , 2 , * , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 1 , 1 , 1 , 11 , 10 , 12 , 13 , 14 , 5 , 1 , 15 , 7 , 16 , 5 , 17 , 18 , 1 , 19 , 20 , 9 , 5 , 21 , 22 , 3 , 17
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          Abstract

          The COVID-19 pandemic highlights the substantial public health, economic, and societal consequences of virus spillover from a wildlife reservoir. Widespread human transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) also presents a new set of challenges when considering viral spillover from people to naïve wildlife and other animal populations. The establishment of new wildlife reservoirs for SARS-CoV-2 would further complicate public health control measures and could lead to wildlife health and conservation impacts. Given the likely bat origin of SARS-CoV-2 and related beta-coronaviruses (β-CoVs), free-ranging bats are a key group of concern for spillover from humans back to wildlife. Here, we review the diversity and natural host range of β-CoVs in bats and examine the risk of humans inadvertently infecting free-ranging bats with SARS-CoV-2. Our review of the global distribution and host range of β-CoV evolutionary lineages suggests that 40+ species of temperate-zone North American bats could be immunologically naïve and susceptible to infection by SARS-CoV-2. We highlight an urgent need to proactively connect the wellbeing of human and wildlife health during the current pandemic and to implement new tools to continue wildlife research while avoiding potentially severe health and conservation impacts of SARS-CoV-2 "spilling back" into free-ranging bat populations.

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          Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China

          Summary Background A recent cluster of pneumonia cases in Wuhan, China, was caused by a novel betacoronavirus, the 2019 novel coronavirus (2019-nCoV). We report the epidemiological, clinical, laboratory, and radiological characteristics and treatment and clinical outcomes of these patients. Methods All patients with suspected 2019-nCoV were admitted to a designated hospital in Wuhan. We prospectively collected and analysed data on patients with laboratory-confirmed 2019-nCoV infection by real-time RT-PCR and next-generation sequencing. Data were obtained with standardised data collection forms shared by WHO and the International Severe Acute Respiratory and Emerging Infection Consortium from electronic medical records. Researchers also directly communicated with patients or their families to ascertain epidemiological and symptom data. Outcomes were also compared between patients who had been admitted to the intensive care unit (ICU) and those who had not. Findings By Jan 2, 2020, 41 admitted hospital patients had been identified as having laboratory-confirmed 2019-nCoV infection. Most of the infected patients were men (30 [73%] of 41); less than half had underlying diseases (13 [32%]), including diabetes (eight [20%]), hypertension (six [15%]), and cardiovascular disease (six [15%]). Median age was 49·0 years (IQR 41·0–58·0). 27 (66%) of 41 patients had been exposed to Huanan seafood market. One family cluster was found. Common symptoms at onset of illness were fever (40 [98%] of 41 patients), cough (31 [76%]), and myalgia or fatigue (18 [44%]); less common symptoms were sputum production (11 [28%] of 39), headache (three [8%] of 38), haemoptysis (two [5%] of 39), and diarrhoea (one [3%] of 38). Dyspnoea developed in 22 (55%) of 40 patients (median time from illness onset to dyspnoea 8·0 days [IQR 5·0–13·0]). 26 (63%) of 41 patients had lymphopenia. All 41 patients had pneumonia with abnormal findings on chest CT. Complications included acute respiratory distress syndrome (12 [29%]), RNAaemia (six [15%]), acute cardiac injury (five [12%]) and secondary infection (four [10%]). 13 (32%) patients were admitted to an ICU and six (15%) died. Compared with non-ICU patients, ICU patients had higher plasma levels of IL2, IL7, IL10, GSCF, IP10, MCP1, MIP1A, and TNFα. Interpretation The 2019-nCoV infection caused clusters of severe respiratory illness similar to severe acute respiratory syndrome coronavirus and was associated with ICU admission and high mortality. Major gaps in our knowledge of the origin, epidemiology, duration of human transmission, and clinical spectrum of disease need fulfilment by future studies. Funding Ministry of Science and Technology, Chinese Academy of Medical Sciences, National Natural Science Foundation of China, and Beijing Municipal Science and Technology Commission.
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            A pneumonia outbreak associated with a new coronavirus of probable bat origin

            Since the outbreak of severe acute respiratory syndrome (SARS) 18 years ago, a large number of SARS-related coronaviruses (SARSr-CoVs) have been discovered in their natural reservoir host, bats 1–4 . Previous studies have shown that some bat SARSr-CoVs have the potential to infect humans 5–7 . Here we report the identification and characterization of a new coronavirus (2019-nCoV), which caused an epidemic of acute respiratory syndrome in humans in Wuhan, China. The epidemic, which started on 12 December 2019, had caused 2,794 laboratory-confirmed infections including 80 deaths by 26 January 2020. Full-length genome sequences were obtained from five patients at an early stage of the outbreak. The sequences are almost identical and share 79.6% sequence identity to SARS-CoV. Furthermore, we show that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus. Pairwise protein sequence analysis of seven conserved non-structural proteins domains show that this virus belongs to the species of SARSr-CoV. In addition, 2019-nCoV virus isolated from the bronchoalveolar lavage fluid of a critically ill patient could be neutralized by sera from several patients. Notably, we confirmed that 2019-nCoV uses the same cell entry receptor—angiotensin converting enzyme II (ACE2)—as SARS-CoV.
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              Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding

              Summary Background In late December, 2019, patients presenting with viral pneumonia due to an unidentified microbial agent were reported in Wuhan, China. A novel coronavirus was subsequently identified as the causative pathogen, provisionally named 2019 novel coronavirus (2019-nCoV). As of Jan 26, 2020, more than 2000 cases of 2019-nCoV infection have been confirmed, most of which involved people living in or visiting Wuhan, and human-to-human transmission has been confirmed. Methods We did next-generation sequencing of samples from bronchoalveolar lavage fluid and cultured isolates from nine inpatients, eight of whom had visited the Huanan seafood market in Wuhan. Complete and partial 2019-nCoV genome sequences were obtained from these individuals. Viral contigs were connected using Sanger sequencing to obtain the full-length genomes, with the terminal regions determined by rapid amplification of cDNA ends. Phylogenetic analysis of these 2019-nCoV genomes and those of other coronaviruses was used to determine the evolutionary history of the virus and help infer its likely origin. Homology modelling was done to explore the likely receptor-binding properties of the virus. Findings The ten genome sequences of 2019-nCoV obtained from the nine patients were extremely similar, exhibiting more than 99·98% sequence identity. Notably, 2019-nCoV was closely related (with 88% identity) to two bat-derived severe acute respiratory syndrome (SARS)-like coronaviruses, bat-SL-CoVZC45 and bat-SL-CoVZXC21, collected in 2018 in Zhoushan, eastern China, but were more distant from SARS-CoV (about 79%) and MERS-CoV (about 50%). Phylogenetic analysis revealed that 2019-nCoV fell within the subgenus Sarbecovirus of the genus Betacoronavirus, with a relatively long branch length to its closest relatives bat-SL-CoVZC45 and bat-SL-CoVZXC21, and was genetically distinct from SARS-CoV. Notably, homology modelling revealed that 2019-nCoV had a similar receptor-binding domain structure to that of SARS-CoV, despite amino acid variation at some key residues. Interpretation 2019-nCoV is sufficiently divergent from SARS-CoV to be considered a new human-infecting betacoronavirus. Although our phylogenetic analysis suggests that bats might be the original host of this virus, an animal sold at the seafood market in Wuhan might represent an intermediate host facilitating the emergence of the virus in humans. Importantly, structural analysis suggests that 2019-nCoV might be able to bind to the angiotensin-converting enzyme 2 receptor in humans. The future evolution, adaptation, and spread of this virus warrant urgent investigation. Funding National Key Research and Development Program of China, National Major Project for Control and Prevention of Infectious Disease in China, Chinese Academy of Sciences, Shandong First Medical University.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS Pathog
                PLoS Pathog
                plos
                plospath
                PLoS Pathogens
                Public Library of Science (San Francisco, CA USA )
                1553-7366
                1553-7374
                3 September 2020
                September 2020
                : 16
                : 9
                : e1008758
                Affiliations
                [1 ] EcoHealth Alliance, New York, New York, United States of America
                [2 ] US Geological Survey, Fort Collins Science Center, Ft. Collins, Colorado, United States of America
                [3 ] US Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America
                [4 ] Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, United States of America
                [5 ] US Geological Survey, National Wildlife Health Center, Madison, Wisconsin, United States of America
                [6 ] Department of Integrative Biology, University of California Berkeley, Berkeley, California, United States of America
                [7 ] Arthropod-borne and Infectious Diseases Laboratory, Department of Microbiology, Immunology & Pathology, College of Veterinary Medicine & Biomedical Sciences, Colorado State University, Ft. Collins, Colorado, United States of America
                [8 ] Wildlife Veterinary Consulting, Livermore, Colorado, United States of America
                [9 ] US Fish and Wildlife Service, Hadley, Massachusetts, United States of America
                [10 ] School of Veterinary Science, University of Queensland, Gatton, Queensland, Australia
                [11 ] Bat Conservation International, Austin, Texas, United States of America
                [12 ] Department of Ecology & Evolutionary Biology, University of California Santa Cruz, Santa Cruz, California, United States of America
                [13 ] US Department of Agriculture, National Wildlife Research Center, Ft. Collins, Colorado, United States of America
                [14 ] School of Veterinary Science, Massey University, Palmerston North, New Zealand
                [15 ] One Health Institute, School of Veterinary Medicine, University of California Davis, Davis, California, United States of America
                [16 ] Department of Biological Sciences, Texas Tech University, Lubbock, Texas, United States of America
                [17 ] Programme in Emerging Infectious Diseases, Duke-National University of Singapore Medical School, Singapore
                [18 ] Environmental Futures Research Institute, Griffith University, Nathan, Australia
                [19 ] Department of Microbiology & Immunology, Montana State University, Bozeman, Montana, United States of America
                [20 ] Department of Biology, Bucknell University, Lewisburg, Pennsylvania, United States of America
                [21 ] Institute of Biodiversity, Animal Health & Comparative Medicine, University of Glasgow, Scotland, United Kingdom
                [22 ] MRC-University of Glasgow Centre for Virus Research, Glasgow, Scotland, United Kingdom
                University of Pittsburgh, UNITED STATES
                Author notes

                The authors have declared that no competing interests exist.

                Author information
                http://orcid.org/0000-0003-3211-1875
                http://orcid.org/0000-0002-2915-8894
                http://orcid.org/0000-0002-4726-2361
                http://orcid.org/0000-0001-6827-8701
                http://orcid.org/0000-0002-1065-9760
                http://orcid.org/0000-0003-4276-073X
                http://orcid.org/0000-0003-0583-2853
                http://orcid.org/0000-0002-2762-947X
                http://orcid.org/0000-0002-2046-5695
                http://orcid.org/0000-0002-1373-9301
                http://orcid.org/0000-0002-4671-7002
                http://orcid.org/0000-0002-9469-1839
                http://orcid.org/0000-0002-8256-0081
                http://orcid.org/0000-0003-0087-3015
                http://orcid.org/0000-0003-4844-7533
                http://orcid.org/0000-0001-6042-2860
                http://orcid.org/0000-0002-4996-915X
                http://orcid.org/0000-0003-3552-5352
                http://orcid.org/0000-0003-4250-6459
                http://orcid.org/0000-0003-3538-3550
                http://orcid.org/0000-0002-3120-4802
                http://orcid.org/0000-0001-8651-2012
                http://orcid.org/0000-0002-4792-2868
                http://orcid.org/0000-0002-9910-6125
                http://orcid.org/0000-0001-7475-2705
                http://orcid.org/0000-0002-6473-3049
                http://orcid.org/0000-0003-2752-0535
                Article
                PPATHOGENS-D-20-01177
                10.1371/journal.ppat.1008758
                7470399
                32881980
                317f7ce5-8838-436c-9d7c-2a0e05b1cb0c

                This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

                History
                Page count
                Figures: 2, Tables: 0, Pages: 19
                Funding
                This work was supported in part by the USGS John Wesley Powell Center for Analysis and Synthesis, National Institute of Allergy and Infectious Diseases of the National Institutes of Health (Award Number R01AI110964), and the US Department of Defense, Defense Threat Reduction Agency (HDTRA11710064). Funding for DTSH was provided by a Royal Society Te Aparangi grant RDF-MAU1701. Funding for DGS was provided by a Wellcome Trust Senior Research Fellowship (217221/Z/19/Z). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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