Emergence of a Severe Acute Respiratory Syndrome Coronavirus 2 virus variant with novel genomic architecture in Hong Kong.
02 Mar 2021-Clinical Infectious Diseases (Oxford University Press (OUP))-Vol. 73, Iss: 9, pp 1696-1699
TL;DR: In this paper, the authors reported the discovery of a SARS-CoV-2 variant with a novel genomic architecture characterized by absent ORF7a, ORF 7b, and ORF8, and a Cterminally modified ORF6 product resulting from partial 5'-untranslated region (UTR) duplication and transposition.
Abstract: Throughout the coronavirus disease 2019 (COVID-19) pandemic, divergent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) lineages have emerged continuously, mostly through the genomic accumulation of substitutions. We report the discovery of a SARS-CoV-2 variant with a novel genomic architecture characterized by absent ORF7a, ORF7b, and ORF8, and a C-terminally modified ORF6 product resulting from partial 5'-untranslated region (UTR) duplication and transposition.
Citations
More filters
K Pollard1, Qun Wang1, Yuguo Li1, David Christopher Lung2, David Christopher Lung3, Pak-To Chan1, Chung-Hin Dung1, Wei Jia1, Te Miao1, Jianxiang Huang1, Wenzhao Chen1, Zixuan Wang1, Kai-Ming Leung4, Zhang Lin5, Daniel Wong1, Herman Tse2, Sally Cheuk-Ying Wong2, Garnet K. Y. Choi2, Jimmy Yiu-Wing Lam6, Kelvin K. W. To7, Vincent C.C. Cheng7, Kwok-Yung Yuen8 •
TL;DR: Wang et al. as discussed by the authors investigated two such outbreaks of COVID-19 in Hong Kong, identified the probable role of chimney effect-induced airflow in a building drainage system in the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and injected tracer gas (SF6) into the drainage stacks via the water closet of the index case.
25 citations
15 Apr 2021
TL;DR: In this paper, the genome sequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains from the clinical samples of three patients in Hong Kong showed a 370 nucleotide deletion resulting in the complete loss of ORF7a.
Abstract: We report the genome sequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains from the clinical samples of three coronavirus disease 2019 (COVID-19) patients in Hong Kong. All the genome sequences showed a 370-nucleotide deletion resulting in the complete loss of ORF7a.
13 citations
TL;DR: In this paper, the authors summarize the S protein mutations detected among coronavirus disease 2019 (COVID-19) patients in Hong Kong in 2020, and the full encoding region of the S proteins was sequenced.
Abstract: In 2020, numerous fast-spreading severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants have been reported. These variants had unusually high genetic changes in the spike (S) protein. In an attempt to understand the genetic background of SARS-CoV-2 viruses in Hong Kong, especially before vaccination, the purpose of this study is to summarize the S protein mutations detected among coronavirus disease 2019 (COVID-19) patients in Hong Kong in 2020. COVID-19 cases were selected every month in 2020. One virus from each case was analyzed. The full encoding region of the S proteins was sequenced. From January 2020 to December 2020, a total of 340 COVID-19 viruses were sequenced. The amino acids of the S protein for 44 (12.9%) were identical to the reference sequence, WIV04 (GenBank accession MN996528). For the remaining 296 sequences (87.1%), a total of 43 nonsynonymous substitution patterns were found. Of the nonsynonymous substitutions found, some of them were only detected at specific time intervals and then they disappeared. The ongoing genetic surveillance system is important. It would facilitate early detection of mutations that can increase infectivity as well as mutations that are selected for the virus to escape immunological restraint.
9 citations
27 Jun 2021
TL;DR: In this paper, a systemic comparison of both viruses' structural and functional characteristics, delineating their distinct strategies for efficient spread, is provided, and the authors conclude that both viruses have a similar appearance as enveloped viruses with positive-stranded RNA and envelope spikes mediating cellular entry, the entry process, downstream biological and immunological pathways, clinical outcomes, and disease courses are strikingly different.
Abstract: SARS-CoV-2 and HIV are zoonotic viruses that rapidly reached pandemic scale, causing global losses and fear. The COVID-19 and AIDS pandemics ignited massive efforts worldwide to develop antiviral strategies and characterize viral architectures, biological and immunological properties, and clinical outcomes. Although both viruses have a comparable appearance as enveloped viruses with positive-stranded RNA and envelope spikes mediating cellular entry, the entry process, downstream biological and immunological pathways, clinical outcomes, and disease courses are strikingly different. This review provides a systemic comparison of both viruses’ structural and functional characteristics, delineating their distinct strategies for efficient spread.
4 citations
S K Sarif Hassan, Kodakandla1, Elrashdy M. Redwan, Kenneth Lundstrom, Pal Choudhury P2, Abd El-Aziz Tm3, Kazuo Takayama4, Ramesh Kandimalla5, Amos Lal6, Ángel Serrano-Aroca7, Gajendra Kumar Azad8, Aljabali Aaa9, Giorgio Palù10, Gaurav Chauhan11, Parise Adadi12, Murtaza M. Tambuwala13, Adam Brufsky14, Wagner Baetas-da-Cruz15, Debmalya Barh16, Nicolas G. Bazan, Vladimir N. Uversky17 •
University of Mumbai1, Indian Statistical Institute2, University of Texas Health Science Center at San Antonio3, Kyoto University4, Indian Institute of Chemical Technology5, Mayo Clinic6, Universidad Católica de Valencia San Vicente Mártir7, Patna University8, Yarmouk University9, University of Padua10, Monterrey Institute of Technology and Higher Education11, University of Otago12, Ulster University13, University of Pittsburgh14, Federal University of Rio de Janeiro15, Universidade Federal de Minas Gerais16, University of South Florida17
TL;DR: In this article, the authors identified 47 unique truncated ORF8 proteins (T-ORF8) due to the Q27STOP mutations were identified among 49055 available B.1.7 SARS-CoV-2 sequences.
Abstract: Open reading frame 8 (ORF8) protein is one of the most evolving accessory proteins in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19). It was previously reported that the ORF8 protein inhibits presentation of viral antigens by the major histocompatibility complex class I (MHC-I) and interacts with host factors involved in pulmonary inflammation. The ORF8 protein assists SARS-CoV-2 to evade immunity and replication. Among many contributing mutations, Q27STOP, a mutation in the ORF8 protein defines the B.1.1.7 lineage of SARS-CoV-2, which is engendering the second wave of COVID-19. In the present study, 47 unique truncated ORF8 proteins (T-ORF8) due to the Q27STOP mutations were identified among 49055 available B.1.1.7 SARS-CoV-2 sequences. The results show that only one of the 47 T-ORF8 variants spread to over 57 geo-locations in North America, and other continents which includes Africa, Asia, Europe and South America. Based on various quantitative features such as amino acid homology, polar/non-polar sequence homology, Shannon entropy conservation, and other physicochemical properties of all specific 47 T-ORF8 protein variants, a collection of nine possible T-ORF8 unique variants were defined. The question of whether T-ORF8 variants work similarly to ORF8 has yet to be investigated. A positive response to the question could exacerbate future COVID-19 waves, necessitating severe containment measures.
2 citations
References
More filters
TL;DR: A rational and dynamic virus nomenclature that uses a phylogenetic framework to identify those lineages that contribute most to active spread and is designed to provide a real-time bird’s-eye view of the diversity of the hundreds of thousands of genome sequences collected worldwide.
Abstract: The ongoing pandemic spread of a new human coronavirus, SARS-CoV-2, which is associated with severe pneumonia/disease (COVID-19), has resulted in the generation of tens of thousands of virus genome sequences. The rate of genome generation is unprecedented, yet there is currently no coherent nor accepted scheme for naming the expanding phylogenetic diversity of SARS-CoV-2. Here, we present a rational and dynamic virus nomenclature that uses a phylogenetic framework to identify those lineages that contribute most to active spread. Our system is made tractable by constraining the number and depth of hierarchical lineage labels and by flagging and delabelling virus lineages that become unobserved and hence are probably inactive. By focusing on active virus lineages and those spreading to new locations, this nomenclature will assist in tracking and understanding the patterns and determinants of the global spread of SARS-CoV-2.
2,093 citations
TL;DR: Insight is provided on SARS-CoV-2 evasion of IFN-I response and its potential impact on viral transmission and pathogenesis.
645 citations
TL;DR: There is little evidence that recombination is favoured by natural selection to create advantageous genotypes or purge deleterious mutations, as predicted if recombination functions as a form of sexual reproduction, and recombination may be a mechanistic by-product of the evolutionary pressures acting on other aspects of virus biology.
Abstract: Recombination occurs in many RNA viruses and can be of major evolutionary significance However, rates of recombination vary dramatically among RNA viruses, which can range from clonal to highly recombinogenic Here, we review the factors that might explain this variation in recombination frequency and show that there is little evidence that recombination is favoured by natural selection to create advantageous genotypes or purge deleterious mutations, as predicted if recombination functions as a form of sexual reproduction Rather, recombination rates seemingly reflect larger-scale patterns of viral genome organization, such that recombination may be a mechanistic by-product of the evolutionary pressures acting on other aspects of virus biology
553 citations
TL;DR: The analysis may facilitate custom-designed antiviral strategies based on the molecular specificities of SARS-CoV-2 in different patients and geographical locations and shows the prevalence of single nucleotide transitions as the major mutational type across the world.
Abstract: The novel respiratory disease COVID-19 has reached the status of worldwide pandemic and large efforts are currently being undertaken in molecularly characterizing the virus causing it, SARS-CoV-2. The genomic variability of SARS-CoV-2 specimens scattered across the globe can underly geographically specific etiological effects. In the present study, we gather the 48,635 SARS-CoV-2 complete genomes currently available thanks to the collection endeavor of the GISAID consortium and thousands of contributing laboratories. We analyzed and annotated all SARS-CoV-2 mutations compared with the reference Wuhan genome NC_045512.2, observing an average of 7.23 mutations per sample. Our analysis shows the prevalence of single nucleotide transitions as the major mutational type across the world. There exist at least three clades characterized by geographic and genomic specificity. In particular, clade G, prevalent in Europe, carries a D614G mutation in the Spike protein, which is responsible for the initial interaction of the virus with the host human cell. Our analysis may facilitate custom-designed antiviral strategies based on the molecular specificities of SARS-CoV-2 in different patients and geographical locations.
494 citations
Lisa Miorin1, Thomas Kehrer1, Maria Teresa Sánchez-Aparicio1, Ke Zhang2, Phillip Cohen1, Roosheel S. Patel1, Anastasija Cupic1, Tadashi Makio3, Menghan Mei4, Elena Moreno1, Oded Danziger1, Kris M. White1, Raveen Rathnasinghe1, Melissa B. Uccellini1, Shengyan Gao2, Teresa Aydillo1, Ignacio Mena1, Xin Yin5, Laura Martin-Sancho5, Nevan J. Krogan6, Nevan J. Krogan7, Nevan J. Krogan1, Sumit K. Chanda5, Michael Schotsaert1, Richard W. Wozniak3, Yi Ren4, Brad R. Rosenberg1, Beatriz M. A. Fontoura2, Adolfo García-Sastre1 •
TL;DR: SARS-CoV-2 is able to efficiently block STAT1 and STAT2 nuclear translocation in order to impair transcriptional induction of IFN-stimulated genes (ISGs).
Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the ongoing coronavirus disease 2019 (COVID-19) pandemic that is a serious global health problem. Evasion of IFN-mediated antiviral signaling is a common defense strategy that pathogenic viruses use to replicate and propagate in their host. In this study, we show that SARS-CoV-2 is able to efficiently block STAT1 and STAT2 nuclear translocation in order to impair transcriptional induction of IFN-stimulated genes (ISGs). Our results demonstrate that the viral accessory protein Orf6 exerts this anti-IFN activity. We found that SARS-CoV-2 Orf6 localizes at the nuclear pore complex (NPC) and directly interacts with Nup98-Rae1 via its C-terminal domain to impair docking of cargo-receptor (karyopherin/importin) complex and disrupt nuclear import. In addition, we show that a methionine-to-arginine substitution at residue 58 impairs Orf6 binding to the Nup98-Rae1 complex and abolishes its IFN antagonistic function. All together our data unravel a mechanism of viral antagonism in which a virus hijacks the Nup98-Rae1 complex to overcome the antiviral action of IFN.
365 citations
Related Papers (5)
Yvonne C. F. Su, Danielle E. Anderson, Barnaby Edward Young, Martin Linster, Feng Zhu, Jayanthi Jayakumar, Yan Zhuang, Shirin Kalimuddin, Shirin Kalimuddin, Jenny G. Low, Jenny G. Low, Chee Wah Tan, Wan Ni Chia, Tze Minn Mak, Sophie Octavia, Jean-Marc Chavatte, Raphael T.C. Lee, Surinder Pada, Seow Yen Tan, Louisa Sun, Gabriel Yan, Sebastian Maurer-Stroh, Sebastian Maurer-Stroh, Ian H. Mendenhall, Yee Sin Leo, David C. Lye, Lin-Fa Wang, Lin-Fa Wang, Gavin J. D. Smith, Gavin J. D. Smith
Yu-Nong Gong, Yu-Nong Gong, Kuo Chien Tsao, Kuo Chien Tsao, Mei Jen Hsiao, Chung Guei Huang, Chung Guei Huang, Peng Nien Huang, Peng Nien Huang, Po Wei Huang, Kuo-Ming Lee, Yi-Chun Liu, Shu Li Yang, Shu Li Yang, Rei-Lin Kuo, Kuan-Fu Chen, Kuan-Fu Chen, Yen Chin Liu, Sheng-Yu Huang, Hsing-I Huang, Ming Tsan Liu, Ji Rong Yang, Cheng-Hsun Chiu, Cheng-Ta Yang, Cheng-Ta Yang, Guang-Wu Chen, Guang-Wu Chen, Shin-Ru Shih