Mosaic Structure of Human Coronavirus NL63, One Thousand Years of Evolution

Pyrć, Krzysztof; Dijkman, Ronald; Deng, Lea; Jebbink, Maarten F.; Ross, Howard A.; Berkhout, Ben; Hoek, Lia van der

doi:10.1016/j.jmb.2006.09.074

Cited by 167 publications

(179 citation statements)

References 52 publications

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“…The estimation of time of divergence was first extensively used in coronaviruses after the SARS epidemic for estimating the date of interspecies jumping of SARSr-CoV from civets to humans and that from BCoV to HCoV-OC43 [31,32]. Subsequently, when various novel human and animal coronaviruses were discovered, evolutionary rates and divergence time in the Coronaviridae family were estimated by various groups using different approaches [31,[33][34][35]. Although Bayesian inference in BEAST is probably the most widely accepted approach and was used by most researchers, the use of different genes (ORF1ab, helicase, S and N genes) and datasets by different groups have resulted in considerable difference in the estimated history of coronaviruses.…”

Section: Evolutionary Rate and Divergencementioning

confidence: 99%

Application of “Omics” to Prion Biomarker Discovery

2014

Omics in Clinical Practice

116

143

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Abstract:The drastic increase in the number of coronaviruses discovered and coronavirus genomes being sequenced have given us an unprecedented opportunity to perform genomics and bioinformatics analysis on this family of viruses. Coronaviruses possess the largest genomes (26.4 to 31.7 kb) among all known RNA viruses, with G + C contents varying from 32% to 43%. Variable numbers of small ORFs are present between the various conserved genes (ORF1ab, spike, envelope, membrane and nucleocapsid) and downstream to nucleocapsid gene in different coronavirus lineages. Phylogenetically, three genera, Alphacoronavirus, Betacoronavirus and Gammacoronavirus, with Betacoronavirus consisting of subgroups A, B, C and D, exist. A fourth genus, Deltacoronavirus, which includes bulbul coronavirus HKU11, thrush coronavirus HKU12 and munia coronavirus HKU13, is emerging. Molecular clock analysis using various gene loci revealed that the time of most recent common ancestor of human/civet SARS related coronavirus to be 1999-2002, with estimated substitution rate of 410 coronavirus HKU1 (HCoV-HKU1). Codon usage bias in coronaviruses were observed, with HCoV-HKU1 showing the most extreme bias, and cytosine deamination and selection of CpG suppressed clones are the two major independent biological forces that shape such codon usage bias in coronaviruses.

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Section: Evolutionary Rate and Divergencementioning

confidence: 99%

Application of “Omics” to Prion Biomarker Discovery

2014

Omics in Clinical Practice

116

143

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“…In fact, recombination has been implicated in the sharing of homologous genes by distantly related members of the Coronaviridae family (14). Phylogenetic analyses have revealed that HCoV-NL63 may have undergone many recombination events, including two sites of recombination in the S gene and potential recombination between HCoV-NL63 and porcine enteric disease virus (PEDV) in the M gene (101). Additionally, evidence suggests that natural avian infectious bronchitis virus (AIBV) isolates recombined with a vaccine strain (Holland 52), specifically in the N gene (102).…”

Section: Recombinationmentioning

confidence: 99%

Coronavirus Host Range Expansion and Middle East Respiratory Syndrome Coronavirus Emergence: Biochemical Mechanisms and Evolutionary Perspectives

Peck¹,

Burch²,

Heise

et al. 2015

Annu. Rev. Virol.

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Coronaviruses have frequently expanded their host range in recent history, with two events resulting in severe disease outbreaks in human populations. Severe acute respiratory syndrome coronavirus (SARS-CoV) emerged in 2003 in Southeast Asia and rapidly spread around the world before it was controlled by public health intervention strategies. The 2012 Middle East respiratory syndrome coronavirus (MERS-CoV) outbreak represents another prime example of virus emergence from a zoonotic reservoir. Here, we review the current knowledge of coronavirus cross-species transmission, with particular focus on MERS-CoV. MERS-CoV is still circulating in the human population, and the mechanisms governing its cross-species transmission have been only partially elucidated, highlighting a need for further investigation. We discuss biochemical determinants mediating MERS-CoV host cell permissivity, including virus spike interactions with the MERS-CoV cell surface receptor dipeptidyl peptidase 4 (DPP4), and evolutionary mechanisms that may facilitate host range expansion, including recombination, mutator alleles, and mutational robustness. Understanding these mechanisms can help us better recognize the threat of emergence for currently circulating zoonotic strains.

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“…Human coronavirus NL63 (HCoV-NL63) is a relatively recently discovered human respiratory pathogen with a high worldwide prevalence (Fouchier et al, 2004;Golda & Pyrc, 2008;Hofmann et al, 2005;Pyrc et al, 2004Pyrc et al, , 2006Pyrc et al, , 2007aPyrc et al, , b, 2008Schildgen et al, 2006;van der Hoek et al, 2004 (Fig. 1a).…”

Section: Introductionmentioning

confidence: 99%

Infection with human coronavirus NL63 enhances streptococcal adherence to epithelial cells

Gołda

Małek

Dudek

et al. 2011

Journal of General Virology

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Understanding the mechanisms of augmented bacterial pathogenicity in post-viral infections is the first step in the development of an effective therapy. This study assessed the effect of human coronavirus NL63 (HCoV-NL63) on the adherence of bacterial pathogens associated with respiratory tract illnesses. It was shown that HCoV-NL63 infection resulted in an increased adherence of Streptococcus pneumoniae to virus-infected cell lines and fully differentiated primary human airway epithelium cultures. The enhanced binding of bacteria correlated with an increased expression level of the platelet-activating factor receptor (PAF-R), but detailed evaluation of the bacterium-PAF-R interaction revealed a limited relevance of this process. INTRODUCTIONThe concept of excessive morbidity and mortality of bacterial infection occurring during or shortly after viral infection was first formulated for influenza virus in the early 19th century. Analysis of influenza pandemics showed that the incidence of bacterial pneumonia was increased and contributed substantially to mortality rates (Abrahams et al., 1919;Muir & Wilson, 1919;Stone & Swift, 1919;Wilson & Steer, 1919). Comparison of bacteriological and virological data from children hospitalized for respiratory disease shows a high degree of occurrence of viral and bacterial infections positively correlating with the severity of illness (Duttweiler et al., 2004;Kneyber et al., 2005;Randolph et al., 2004;Thorburn et al., 2006). Although the role of a preceding viral infection in development and severity of bacterial respiratory diseases is a clinically welldocumented phenomenon, the exact mechanism has not been elucidated fully.Initially, it was proposed that respiratory viruses facilitate bacterial colonization through physical damage of the respiratory tract epithelium, with exposed basement membrane components being responsible for increased bacterial adherence (Louria et al., 1959;Muir & Wilson, 1919;Wilson & Steer, 1919;Wolbach, 1919). Such a mechanism undoubtedly occurs for highly pathogenic viral species, but it does not explain the occurrence of increased severity of bacterial infection during and shortly after relatively mild viral infections. Analysis of published data suggests that interplay between viruses and bacteria is a complex process, where the final outcome depends heavily on multiple factors, including modulation of innate immune responses resulting in delayed clearance of bacteria, hypersensitization of infected cells leading to enhanced immune-mediated lung damage and modulation of bacterial adherence (Okamoto et al., 2004). The increase in bacterial adherence occurs due to exposure of novel binding sites for bacteria on the epithelial surface, either by expression of highly glycosylated viral proteins (McCullers & Bartmess, 2003;Peltola & McCullers, 2004) or by the alteration of a bacterial receptor expression pattern (McCullers & Rehg, 2002;Patel et al., 1995;Terajima et al., 1997).Bacterial pathogens predominantly involved in secondary infection of the r...

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Mosaic Structure of Human Coronavirus NL63, One Thousand Years of Evolution

Cited by 167 publications

References 52 publications

Application of “Omics” to Prion Biomarker Discovery

Application of “Omics” to Prion Biomarker Discovery

Coronavirus Host Range Expansion and Middle East Respiratory Syndrome Coronavirus Emergence: Biochemical Mechanisms and Evolutionary Perspectives

Infection with human coronavirus NL63 enhances streptococcal adherence to epithelial cells

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