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Date of origin of the SARS coronavirus strains
Hongchao Lu, Yi Zhao, Jingfen Zhang, Yuelan Wang, Wei Li, Xiaopeng Zhu, Shiwei Sun, Jingyi Xu, Lunjiang Ling, Lun Cai, Dongbo Bu, Runsheng Chen
BMC Infectious Diseases , 2004, DOI: 10.1186/1471-2334-4-3
Abstract: We propose a mathematical model to estimate the evolution rate of the SARS coronavirus genome and the time of the last common ancestor of the sequenced SARS strains. Under some common assumptions and justifiable simplifications, a few simple equations incorporating the evolution rate (K) and time of the last common ancestor of the strains (T0) can be deduced. We then implemented the least square method to estimate K and T0 from the dataset of sequences and corresponding times. Monte Carlo stimulation was employed to discuss the results.Based on 6 strains with accurate dates of host death, we estimated the time of the last common ancestor to be about August or September 2002, and the evolution rate to be about 0.16 base/day, that is, the SARS coronavirus would on average change a base every seven days. We validated our method by dividing the strains into two groups, which coincided with the results from comparative genomics.The applied method is simple to implement and avoid the difficulty and subjectivity of choosing the root of phylogenetic tree. Based on 6 strains with accurate date of host death, we estimated a time of the last common ancestor, which is coincident with epidemic investigations, and an evolution rate in the same range as that reported for the HIV-1 virus.A new respiratory infectious epidemic, severe acute respiratory syndrome (SARS), broke out and spread throughout the world, affecting over 8,000 individuals in 32 countries[1,2]. In response to this outbreak, a global network of international collaborating laboratories was immediately sponsored and established by World Health Organization (WHO) to facilitate the identification of the causative agent of SARS. By now the putative pathogen of SARS has been identified, by experimental proof and by Koch's postulates, as a new coronavirus, a single positive-strand RNA virus [3-5]]. The whole genome of SARS coronavirus was first sequenced by the British Columbia Centre for Disease Control (CDC) in Canada
WHO says coronavirus causes SARS
Robert Walgate
Genome Biology , 2003, DOI: 10.1186/gb-spotlight-20030417-01
Abstract: The organization claimed that its collaborating laboratories have concluded the coronavirus meets all four of "Koch's postulates" for a causative agent: it must be found in all cases of the disease, it must be isolated from the host and grown in pure culture, it must reproduce the original disease when introduced into a susceptible host, and it must be found in the experimental host so infected.The key to this announcement were the last two tests, performed in monkeys by Albert Osterhaus and colleagues at the Erasmus Medical Centre in Rotterdam, one of WHO's global collaborative research network, which now consists of 13 laboratories.Klaus St?hr, WHO virologist and the coordinator of the network, said at a press conference today, "The people in this network have put aside profit and prestige to work together to find the cause of this new disease and to find new ways of fighting it… In this globalized world, such collaboration is the only way forward in tackling emerging diseases."On April 12, the 29,736-nucleotide genome sequence of the virus was completed by a team at the Michael Smith Genome Sciences Centre in Vancouver, which was not a formal member of the network. The US Centers for Disease Control (CDC), part of the network, followed two days later by publishing its own sequence, slightly shorter at 29,727 nucleotides but otherwise differing by only "about ten base-pairs, a trivial difference," according to Julie Gerberding, director of the CDC.As the Canadian samples, purified at Canada's National Microbiology Laboratory in Winnipeg from SARS cases in Toronto, are so similar to the CDC's, which came directly from Asia, the likelihood is that this virus was brought from Hong Kong to Toronto by the Canadian index case. This was an elderly woman who had stayed at a Hong Kong hotel on the same floor as an infected doctor from Guandong in South China, where the disease seems to have originated.One question still open is whether this coronavirus is truly the only vi
Design and application of 60mer oligonucleotide microarray in SARS coronavirus detection
SHI Rong,Ma Wenli,WU Qinghua,ZHANG Bao,Song Yanbin,GUO Qiuye,Xiao Weiwei,WANG Yan,Zheng Wenling,
SHI Rong
,MA Wenli,WU Qinghua,ZHANG Bao,SONG Yanbin,GUO Qiuye,XIAO Weiwei,WANG Yan & ZHENG Wenling . Institute of Molecular Biology,First Military Medical University,Guangzhou,China,.

科学通报(英文版) , 2003,
Abstract: In April 2003, a novel coronavirus1,2] which was associated with cases of Severe Acute Respiratory Syn-drome (SARS) was first isolated and sequenced in Canada. The genome of SARS coronavirus (SARS-CoV) is 297273] nucleotides in length and has 11 known open reading frames (ORFs). Although the genome organiza-tion of this virus is similar to that of other coronaviruses, phylogenetic analyses and sequence alignment show that SARS-CoV is not closely related to any of the previously ch…
Inhibition of cytokine gene expression and induction of chemokine genes in non-lymphatic cells infected with SARS coronavirus
Martin Spiegel, Friedemann Weber
Virology Journal , 2006, DOI: 10.1186/1743-422x-3-17
Abstract: A comparison with established cytokine-inducing viruses revealed that SARS-CoV only weakly triggered a cytokine response. In particular, SARS-CoV did not activate significant transcription of the interferons IFN-α, IFN-β, IFN-λ1, IFN-λ2/3, as well as of the interferon-induced antiviral genes ISG56 and MxA, the chemokine RANTES and the interleukine IL-6. Interestingly, however, SARS-CoV strongly induced the chemokines IP-10 and IL-8 in the colon carcinoma cell line Caco-2, but not in the embryonic kidney cell line 293.Our data indicate that SARS-CoV suppresses the antiviral cytokine system of non-immune cells to a large extent, thus buying time for dissemination in the host. However, synthesis of IP-10 and IL-8, which are established markers for acute-stage SARS, escapes the virus-induced silencing at least in some cell types. Therefore, the progressive infiltration of immune cells into the infected lungs observed in SARS patients could be due to the production of these chemokines by the infected tissue cells.For most viruses, the initial encounter with the host takes place in cells of non-lymphatic origin. The outcome of this primary infection can determine the course of disease, and the cytokine response of the infected cell plays a vital part. Type I interferons (IFN-α/β) are potent, antivirally active cytokines which can be produced by most, if not all, body cells in response to virus infection. IFNs not only trigger the synthesis of antivirally active proteins, they also activate the innate immune system and help to shape adaptive immunity [1]. Other virus-induced cytokines and chemokines activate the adaptive immune system and direct the migration of leukocytes [2]. Viruses, on the other hand, have evolved various mechanisms to counteract the host's cytokine response [3], and their ability to induce or inhibit cytokine production in infected cells has direct consequences for the balance between host defense and virus propagation.SARS coronavirus (SARS-CoV) is t
Dynamic Innate Immune Responses of Human Bronchial Epithelial Cells to Severe Acute Respiratory Syndrome-Associated Coronavirus Infection  [PDF]
Tomoki Yoshikawa,Terence E. Hill,Naoko Yoshikawa,Vsevolod L. Popov,Cristi L. Galindo,Harold R. Garner,C. J. Peters,Chien-Te (Kent) Tseng
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0008729
Abstract: Human lung epithelial cells are likely among the first targets to encounter invading severe acute respiratory syndrome-associated coronavirus (SARS-CoV). Not only can these cells support the growth of SARS-CoV infection, but they are also capable of secreting inflammatory cytokines to initiate and, eventually, aggravate host innate inflammatory responses, causing detrimental immune-mediated pathology within the lungs. Thus, a comprehensive evaluation of the complex epithelial signaling to SARS-CoV is crucial for paving the way to better understand SARS pathogenesis. Based on microarray-based functional genomics, we report here the global gene response of 2B4 cells, a cloned bronchial epithelial cell line derived from Calu-3 cells. Specifically, we found a temporal and spatial activation of nuclear factor (NF)κB, activator protein (AP)-1, and interferon regulatory factor (IRF)-3/7 in infected 2B4 cells at 12-, 24-, and 48-hrs post infection (p.i.), resulting in the activation of many antiviral genes, including interferon (IFN)-β, -λs, inflammatory mediators, and many IFN-stimulated genes (ISGs). We also showed, for the first time, that IFN-β and IFN-λs were capable of exerting previously unrecognized, non-redundant, and complementary abilities to limit SARS-CoV replication, even though their expression could not be detected in infected 2B4 bronchial epithelial cells until 48 hrs p.i. Collectively, our results highlight the mechanics of the sequential events of antiviral signaling pathway/s triggered by SARS-CoV in bronchial epithelial cells and identify novel cellular targets for future studies, aiming at advancing strategies against SARS.
The Effects of Temperature and Relative Humidity on the Viability of the SARS Coronavirus  [PDF]
K. H. Chan,J. S. Malik Peiris,S. Y. Lam,L. L. M. Poon,K. Y. Yuen,W. H. Seto
Advances in Virology , 2011, DOI: 10.1155/2011/734690
Abstract: The main route of transmission of SARS CoV infection is presumed to be respiratory droplets. However the virus is also detectable in other body fluids and excreta. The stability of the virus at different temperatures and relative humidity on smooth surfaces were studied. The dried virus on smooth surfaces retained its viability for over 5 days at temperatures of 22–25°C and relative humidity of 40–50%, that is, typical air-conditioned environments. However, virus viability was rapidly lost (>3 log10) at higher temperatures and higher relative humidity (e.g., 38°C, and relative humidity of >95%). The better stability of SARS coronavirus at low temperature and low humidity environment may facilitate its transmission in community in subtropical area (such as Hong Kong) during the spring and in air-conditioned environments. It may also explain why some Asian countries in tropical area (such as Malaysia, Indonesia or Thailand) with high temperature and high relative humidity environment did not have major community outbreaks of SARS. 1. Introduction Severe acute respiratory syndrome (SARS), was a new emerging disease associated with severe pneumonia and spread to involve over 30 countries in 5 continents in 2003. A novel coronavirus was identified as its cause [1–3]. SARS had a dramatic impact on health care services and economies of affected countries, and the overall mortality rate was estimated to be 9%, but rising to 50% in those aged 60 or above [4]. A notable feature of this disease was its predilection for transmission in the health care setting and to close family and social contacts. The disease is presumed to be spread by droplets, close direct or indirect contact, but the relative importance of these routes of transmission is presently unclear. A study showed that viral aerosol generation by a patient with SARS was possible and therefore airborne droplet transmission was a possible means of transmission [5]. However, the role of fomites and environmental contamination in transmission of infection is presently still unclear. An outbreak of disease affecting over 300 residents in high-rise apartment block (Amoy Gardens) in Hong Kong could not be explained by respiratory droplet transmission from infected patients [6]. Infectious virus is detectable in the faeces [7], and aerosolization of virus in contaminated faeces is believed to be the mode of transmission of this outbreak [8]. We and others have reported that infectivity of SARS CoV (SARS coronavirus) was lost after heating at 56°C for 15 minutes but that it was stable for at least 2 days
SARS Coronavirus 3b Accessory Protein Modulates Transcriptional Activity of RUNX1b  [PDF]
Bhavna Varshney, Sudhakar Agnihotram, Yee-Joo Tan, Ralph Baric, Sunil K. Lal
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0029542
Abstract: Background The causative agent of severe acute respiratory syndrome, SARS coronavirus (SARS-CoV) genome encodes several unique group specific accessory proteins with unknown functions. Among them, accessory protein 3b (also known as ORF4) was lately identified as one of the viral interferon antagonist. Recently our lab uncovered a new role for 3b in upregulation of AP-1 transcriptional activity and its downstream genes. Thus, we believe that 3b might play an important role in SARS-CoV pathogenesis and therefore is of considerable interest. The current study aims at identifying novel host cellular interactors of the 3b protein. Methodology/Principal Findings In this study, using yeast two-hybrid and co-immunoprecipitation techniques, we have identified a host transcription factor RUNX1b (Runt related transcription factor, isoform b) as a novel interacting partner for SARS-CoV 3b protein. Chromatin immunoprecipitaion (ChIP) and reporter gene assays in 3b expressing jurkat cells showed recruitment of 3b on the RUNX1 binding element that led to an increase in RUNX1b transactivation potential on the IL2 promoter. Kinase assay and pharmacological inhibitor treatment implied that 3b also affect RUNX1b transcriptional activity by regulating its ERK dependent phosphorylation levels. Additionally, mRNA levels of MIP-1α, a RUNX1b target gene upregulated in SARS-CoV infected monocyte-derived dendritic cells, were found to be elevated in 3b expressing U937 monocyte cells. Conclusions/Significance These results unveil a novel interaction of SARS-CoV 3b with the host factor, RUNX1b, and speculate its physiological relevance in upregulating cytokines and chemokine levels in state of SARS virus infection.
Distinct Patterns of IFITM-Mediated Restriction of Filoviruses, SARS Coronavirus, and Influenza A Virus  [PDF]
I-Chueh Huang ,Charles C. Bailey,Jessica L. Weyer,Sheli R. Radoshitzky,Michelle M. Becker,Jessica J. Chiang,Abraham L. Brass,Asim A. Ahmed,Xiaoli Chi,Lian Dong,Lindsay E. Longobardi,Dutch Boltz,Jens H. Kuhn,Stephen J. Elledge,Sina Bavari,Mark R. Denison,Hyeryun Choe,Michael Farzan
PLOS Pathogens , 2011, DOI: 10.1371/journal.ppat.1001258
Abstract: Interferon-inducible transmembrane proteins 1, 2, and 3 (IFITM1, 2, and 3) are recently identified viral restriction factors that inhibit infection mediated by the influenza A virus (IAV) hemagglutinin (HA) protein. Here we show that IFITM proteins restricted infection mediated by the entry glycoproteins (GP1,2) of Marburg and Ebola filoviruses (MARV, EBOV). Consistent with these observations, interferon-β specifically restricted filovirus and IAV entry processes. IFITM proteins also inhibited replication of infectious MARV and EBOV. We observed distinct patterns of IFITM-mediated restriction: compared with IAV, the entry processes of MARV and EBOV were less restricted by IFITM3, but more restricted by IFITM1. Moreover, murine Ifitm5 and 6 did not restrict IAV, but efficiently inhibited filovirus entry. We further demonstrate that replication of infectious SARS coronavirus (SARS-CoV) and entry mediated by the SARS-CoV spike (S) protein are restricted by IFITM proteins. The profile of IFITM-mediated restriction of SARS-CoV was more similar to that of filoviruses than to IAV. Trypsin treatment of receptor-associated SARS-CoV pseudovirions, which bypasses their dependence on lysosomal cathepsin L, also bypassed IFITM-mediated restriction. However, IFITM proteins did not reduce cellular cathepsin activity or limit access of virions to acidic intracellular compartments. Our data indicate that IFITM-mediated restriction is localized to a late stage in the endocytic pathway. They further show that IFITM proteins differentially restrict the entry of a broad range of enveloped viruses, and modulate cellular tropism independently of viral receptor expression.
Metagenomic Analysis of the Ferret Fecal Viral Flora  [PDF]
Saskia L. Smits, V. Stalin Raj, Minoushka D. Oduber, Claudia M. E. Schapendonk, Rogier Bodewes, Lisette Provacia, Koert J. Stittelaar, Albert D. M. E. Osterhaus, Bart L. Haagmans
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0071595
Abstract: Ferrets are widely used as a small animal model for a number of viral infections, including influenza A virus and SARS coronavirus. To further analyze the microbiological status of ferrets, their fecal viral flora was studied using a metagenomics approach. Novel viruses from the families Picorna-, Papilloma-, and Anelloviridae as well as known viruses from the families Astro-, Corona-, Parvo-, and Hepeviridae were identified in different ferret cohorts. Ferret kobu- and hepatitis E virus were mainly present in human household ferrets, whereas coronaviruses were found both in household as well as farm ferrets. Our studies illuminate the viral diversity found in ferrets and provide tools to prescreen for newly identified viruses that potentially could influence disease outcome of experimental virus infections in ferrets.
Bioinformatics analysis of SARS coronavirus genome polymorphism
Gordana M Pavlovi?-La?eti?, Nenad S Miti?, Milo? V Beljanski
BMC Bioinformatics , 2004, DOI: 10.1186/1471-2105-5-65
Abstract: The nucleotide structure of all 38 isolates is presented. Based on insertions and deletions and dissimilarity due to SNPs, the dataset of all the isolates has been qualitatively classified into three groups each having their own subgroups. These are the A-group with "regular" isolates (no insertions / deletions except for 5' and 3' ends), the B-group of isolates with "long insertions", and the C-group of isolates with "many individual" insertions and deletions. The isolate with the smallest average number of SNPs, compared to other isolates, has been identified (TWH). The density distribution of SNPs, insertions and deletions for each group or subgroup, as well as cumulatively for all the isolates is also presented, along with the gene map for TWH.Since individual SNPs may have occurred at random, positions corresponding to multiple SNPs (occurring in two or more isolates) are identified and presented. This result revises some previous results of a similar type. Amino acid changes caused by multiple SNPs are also identified (for the annotated sequences, as well as presupposed amino acid changes for non-annotated ones). Exact SNP positions for the isolates in each group or subgroup are presented. Finally, a phylogenetic tree for the SARS-CoV isolates has been produced using the CLUSTALW program, showing high compatibility with former qualitative classification.The comparative study of SARS-CoV isolates provides essential information for genome polymorphism, indication of strain differences and variants evolution. It may help with the development of effective treatment.Severe Acute Respiratory Syndrome (SARS) is a new infectious disease reported first in the autumn of 2002 and diagnosed for the first time in March 2003 [1]. It is still a serious threat to human health and SARS coronavirus (CoV) has been associated with the pathogenesis of SARS according to Koch's postulate [2].Significant research efforts have been made into investigation of the SARS-CoV genome sequen
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