Molecular Biology of the SARS-Coronavirus

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Round-table discussion on newly emerging infectious diseases Chairperson: H. Limited variation in SARS coronavirus S and N protein genes observed by direct sequencing from patients' orginal clinical specimens. The Movies can be viewed with Quicktime. SARS Conference. These efforts resulted in two intriguing observations. Secondly, the presence of N-terminal extensions other than nsp7, such as ubiquitin and His 6 , severely affected the primer extension activity of nsp8 Figure 7 , potentially by changing its oligomeric state Figure 2.

However, the relatively strong activity of nsp Figure 7 , a potential naturally occurring replicase processing intermediate, implies that nsp8's activity is unlikely to be directly controlled by an N-terminal cleavage event, as was observed for, e.

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In addition, these observations suggest that a more diverse array of nsp8-containing RdRps may be involved in CoV replication and transcription. Fourthly and last, we observe that a ratio of nsp7:nsp8 is sufficient to capture all nsp8 in a higher molecular weight complex Figure 2 F whereas previously a ratio was required 13 , potentially due to the additional N-terminal residues that altered the dynamics of complex formation.

The functional implications of these observations are not clear at present, but additional structural studies will likely be required to address these issues in detail, and gain insights that may aid in explaining the in vitro results presented here. In addition, our experiments and controls revealed and address a number of disparities between previous claims and hypotheses 12 , and our own observations. Consequently, it is now a distinct possibility that CoV RNA synthesis involves structurally different and functionally separable RNA synthesising complexes [e. It will therefore be crucial to study whether these different polymerase activities are part of the same enzyme complex and, if so, whether they can influence each other's activity or are subject to additional control mechanisms.

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The molecular biology of SARS coronavirus.

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The Molecular Biology of SARS Coronavirus

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Molecular Biology Of The Sars-Coronavirus

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  1. Molecular Biology of the Sars-Coronavirus by Sunil K. Lal | | Booktopia.
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    Molecular Biology of the SARS-Coronavirus

    Figure 1. View large Download slide. Table 1. View Large. Figure 2. Figure 3. Figure 4. Figure 5. Figure 6. Figure 7. Search ADS. Mutation of the aspartic acid residues of the GDD sequence motif of poliovirus RNA-dependent RNA polymerase results in enzymes with altered metal ion requirements for activity. Molecular model of SARS coronavirus polymerase: implications for biochemical functions and drug design.

    Google Preview. Unique and conserved features of genome and proteome of SARS-coronavirus, an early split-off from the coronavirus group 2 lineage.

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    A new lead for nonpeptidic active-site-directed inhibitors of the severe acute respiratory syndrome coronavirus main protease discovered by a combination of screening and docking methods. Coronavirus genome: prediction of putative functional domain in the non-structural polyprotein by comparitive amino acid sequence analysis. Origin and evolution of the archeo-eukaryotic primase superfamily and related palm-domain proteins: structural insights and new members. The broad-spectrum antiviral ribonucleoside ribavirin is an RNA virus mutagen.

    Inhibitory effect of mizoribine and ribavirin on the replication of severe acute respiratory syndrome SARS -associated coronavirus. Ribavirin and interferon-beta synergistically inhibit SARS-associated coronavirus replication in animal and human cell lines. Ovarian tumor domain-containing viral proteases evade ubiquitin- and ISGdependent innate immune responses. The coronavirus replicase: insights into a sophisticated enzyme machinery. Multiple enzymatic activities associated with severe acute respiratory syndrome coronavirus helicase.

    Processing of open reading frame 1a replicase proteins nsp7 to nsp10 in murine hepatitis virus strain A59 replication.

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    Present address: Sjoerd H. Published by Oxford University Press. Issue Section:. Download all figures. Supplementary data. Supplementary Data. Comments 0. Add comment Close comment form modal. Increasing af?

    SARS Conference

    Once such a virus jumped species and attacked humans, the increased human mobility allowed the virus the opportunity for rapid spread. An infected patient from Guangdong who stayed for one day at a hotel in Hong Kong led to the transmission of the disease to 16 other guests who travelled on to seed outbreaks of the disease in Toronto, Singapore, and Vietnam, as well as within Hong Kong itself. The virus exploited the practices used in modern intensive care of patients with severe respiratory disease and the weakness in infection control practices within our health care systems to cause outbreaks within hospitals, further amplifying the spread of the disease.

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