Expression and functional characterization of the putative protein 8b of the severe acute respiratory syndrome‐associated coronavirus

Law, Pui Ying Peggy; Liu, Yuet Man; Geng, Hua; Kwan, Ka Ho; Waye, Mary Miu Yee; Ho, Yu‐Ling

doi:10.1016/j.febslet.2006.05.051

Cited by 28 publications

(32 citation statements)

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“…Although SARS-CoV 8b gene product could be expressed in vivo when cloned directly behind a promoter [11][12][13]; the expression of 8a and 8b in SARS-CoVinfected cells is still controversial [9,10,13]. As shown above, we were unable to detect the protein expression of sgRNA 8 with the 5 0 viral leader sequence, which corroborated with a recent report on ORF8 expression [13].…”

Section: Resultssupporting

confidence: 90%

“…Ten sgRNAs have been identified [5] and the SARS-CoV accessory proteins 3a, 3b, 6,7a, and 7b can be detected in infected cells or SARS patients besides structural proteins [7,8], while the expression of 8a and 8b is controversial [9][10][11][12][13]. Elucidation of the regulatory mechanism in the translation is important for understanding the pathogenesis of SARS-CoV; however, it is hard to compare the differential translation of sgRNAs because the steady-state level of viral proteins in infected cells reflects the sum of transcription, translation, and the relative stabilities of these transcriptional and translational products.…”

Section: Resultsmentioning

confidence: 99%

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Translational control of the subgenomic RNAs of severe acute respiratory syndrome coronavirus

et al. 2009

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The 3'-one-third of the severe acute respiratory syndrome coronavirus (SARS-CoV) genome contains genes for four essential structural proteins and eight virus-specific genes. The expression of this genomic information of SARS-CoV involves synthesis of a nested set of subgenomic RNAs (sgRNAs). In this study, we showed that the translational levels of 10 SARS-CoV sgRNAs including the two low-abundance sgRNAs 2-1 and 3-1 varied considerably in translation reporter assays. We also demonstrated that the initiator AUG codon of sgRNA-8 was silent and the repressive control was most likely positioned in the upstream untranslated region (UTR) of sgRNA-8. The initiator AUG codons of most sgRNAs are in poor Kozak contexts and the translation of truncated proteins from downstream AUG codons by leaky scanning was common in our experimental settings. No significant correlation was found between complexity of 5'-UTR and the sequence context of AUG codon with the level of translation of SARS-CoV sgRNAs. These results will be helpful for further studies to reveal the biological functions and translation regulatory mechanisms of sgRNAs in the coronavirus life cycle and pathogenesis.

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Section: Resultssupporting

confidence: 90%

Section: Resultsmentioning

confidence: 99%

Translational control of the subgenomic RNAs of severe acute respiratory syndrome coronavirus

et al. 2009

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“…When overexpressed, the 9.6 kDa ORF8b localizes to both the nucleus and cytoplasm of Vero E6 and CHO cells [120]. In another study, however, ORF8b was not detected in SARS-CoV-infected cells or when expressed from mRNA's mimicking mRNA8.…”

Section: Sars Accessory Proteinsmentioning

confidence: 99%

“…In another study, however, ORF8b was not detected in SARS-CoV-infected cells or when expressed from mRNA's mimicking mRNA8. However, after it was cloned immediately downstream of a T7 promoter, a soluble, unmodified and monomeric ORF8b protein was expressed in the cytoplasm, which was extremely unstable and rapidly degraded [120]. Similarly, in the absence of the ORF8a region, ORF8b undergoes rapid degradation by proteasomes [116].…”

Section: Sars Accessory Proteinsmentioning

confidence: 99%

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The Role of Severe Acute Respiratory Syndrome (SARS)-Coronavirus Accessory Proteins in Virus Pathogenesis

McBride

Fielding

2012

Viruses

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A respiratory disease caused by a novel coronavirus, termed the severe acute respiratory syndrome coronavirus (SARS-CoV), was first reported in China in late 2002. The subsequent efficient human-to-human transmission of this virus eventually affected more than 30 countries worldwide, resulting in a mortality rate of ~10% of infected individuals. The spread of the virus was ultimately controlled by isolation of infected individuals and there has been no infections reported since April 2004. However, the natural reservoir of the virus was never identified and it is not known if this virus will re-emerge and, therefore, research on this virus continues. The SARS-CoV genome is about 30 kb in length and is predicted to contain 14 functional open reading frames (ORFs). The genome encodes for proteins that are homologous to known coronavirus proteins, such as the replicase proteins (ORFs 1a and 1b) and the four major structural proteins: nucleocapsid (N), spike (S), membrane (M) and envelope (E). SARS-CoV also encodes for eight unique proteins, called accessory proteins, with no known homologues. This review will summarize the current knowledge on SARS-CoV accessory proteins and will include: (i) expression and processing; (ii) the effects on cellular processes; and (iii) functional studies.

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Molecular Biology of the SARS-Coronavirus

Lal

2010

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The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use.Cover Illustration: 3D model of SARS-CoV, with a wedge cut out of it to reveal the nucleocapsid (see Chap. 3 by Daniel R. Beniac and Timothy F. Booth)Background: HL-CZ cells transfected with SARS-CoV Spike construct and incubated with anti-Spike human monoclonal antibody followed by secondary FITC-labeled anti-human antibody (see Chap. 18 by T. Narasaraju, P.L. Soong, J. ter Meulen, J. Goudsmit and Vincent T.K. Chow)Cover design: WMXDesign GmbH, Heidelberg, GermanyPrinted on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com) Foreword SARS was the first new plague of the twenty-first century. Within months, it spread worldwide from its "birthplace" in Guangdong Province, China, affecting over 8,000 people in 25 countries and territories across five continents. SARS exposed the vulnerability of our modern globalised world to the spread of a new emerging infection. SARS (or a similar new emerging disease) could neither have spread so rapidly nor had such a great global impact even 50 years ago, and arguably, it was itself a product of our global inter-connectedness. Increasing affluence and a demand for wild-game as exotic food led to the development of large trade of live animal and game animal markets where many species of wild and domestic animals were co-housed, providing the ideal opportunities for inter-species transmission of viruses and other microbes. 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. Health-care itself has become a two-edged sword.While SARS exposed the vulnerabilities of the modern human condition, it also highlighted the global capacity for a rapid public health and scientific response to an emerging infectious disease threat. Public health and scientific responses succeeded in identifying the causative agent, developing diagnostic tests, and interrupting the spread of the outbreak. The complete virus genome was fully deciphered within weeks and in the ensuing months and years saw an outpouring of scientific research about the disease and its causative agent, the SARS coronavirus. The natural animal reservoir (bats) and amplifier hosts were defined, the virus receptor on human cell...

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Expression and functional characterization of the putative protein 8b of the severe acute respiratory syndrome‐associated coronavirus

Cited by 28 publications

References 26 publications

Translational control of the subgenomic RNAs of severe acute respiratory syndrome coronavirus

Translational control of the subgenomic RNAs of severe acute respiratory syndrome coronavirus

The Role of Severe Acute Respiratory Syndrome (SARS)-Coronavirus Accessory Proteins in Virus Pathogenesis

Molecular Biology of the SARS-Coronavirus

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