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O'Toole, A.; Hill, V.; Pybus, O. G.; Watts, A.; Bogoch, II, Khan, K.; Messina, J. P.; consortium, Covid- Genomics UK, Network for Genomic Surveillance in South, Africa, Brazil, U. K. Cadde Genomic Network, Tegally, H.; Lessells, R. R.; Giandhari, J.; Pillay, S.; Tumedi, K. A.; Nyepetsi, G.; Kebabonye, M.; Matsheka, M.; Mine, M.; Tokajian, S.; Hassan, H.; Salloum, T.; Merhi, G.; Koweyes, J.; Geoghegan, J. L.; de Ligt, J.; Ren, X.; Storey, M.; Freed, N. E.; Pattabiraman, C.; Prasad, P.; Desai, A. S.; Vasanthapuram, R.; Schulz, T. F.; Steinbruck, L.; Stadler, T.; Swiss Viollier Sequencing, Consortium, Parisi, A.; Bianco, A.; Garcia de Viedma, D.; Buenestado-Serrano, S.; Borges, V.; Isidro, J.; Duarte, S.; Gomes, J. P.; Zuckerman, N. S.; Mandelboim, M.; Mor, O.; Seemann, T.; Arnott, A.; Draper, J.; Gall, M.; Rawlinson, W.; Deveson, I.; Schlebusch, S.; McMahon, J.; Leong, L.; Lim, C. K.; Chironna, M.; Loconsole, D.; Bal, A.; Josset, L.; Holmes, E.; St George, K.; Lasek-Nesselquist, E.; Sikkema, R. S.; Oude Munnink, B.; Koopmans, M.; Brytting, M.; Sudha Rani, V.; Pavani, S.; Smura, T.; Heim, A.; Kurkela, S.; Umair, M.; Salman, M.; Bartolini, B.; Rueca, M.; Drosten, C.; Wolff, T.; Silander, O.; Eggink, D.; Reusken, C.; Vennema, H.; Park, A.; Carrington, C.; Sahadeo, N.; Carr, M.; Gonzalez, G.; Diego, Search Alliance San, National Virus Reference, Laboratory, Seq, Covid Spain, Danish Covid-19 Genome, Consortium, Communicable Diseases Genomic, Network, Dutch National, Sars-CoV-surveillance program, Division of Emerging Infectious, Diseases, de Oliveira, T.; Faria, N.; Rambaut, A.; Kraemer, M. U. G..
Wellcome Open Research ; 6:121, 2021.
Article in English | MEDLINE | ID: covidwho-1450989

ABSTRACT

Late in 2020, two genetically-distinct clusters of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) with mutations of biological concern were reported, one in the United Kingdom and one in South Africa. Using a combination of data from routine surveillance, genomic sequencing and international travel we track the international dispersal of lineages B.1.1.7 and B.1.351 (variant 501Y-V2). We account for potential biases in genomic surveillance efforts by including passenger volumes from location of where the lineage was first reported, London and South Africa respectively. Using the software tool grinch (global report investigating novel coronavirus haplotypes), we track the international spread of lineages of concern with automated daily reports, Further, we have built a custom tracking website (cov-lineages.org/global_report.html) which hosts this daily report and will continue to include novel SARS-CoV-2 lineages of concern as they are detected.

2.
New Microbes New Infect ; 41: 100853, 2021 May.
Article in English | MEDLINE | ID: covidwho-1104189

ABSTRACT

The pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing coronavirus disease 2019 (COVID-19), resulting in acute respiratory disease, is a worldwide emergency. Because recently it has been found that SARS-CoV is dependent on host transcription factors (TF) to express the viral genes, efforts are required to understand the molecular interplay between virus and host response. By bioinformatic analysis, we investigated human TF that can bind the SARS-CoV-2 sequence and can be involved in viral transcription. In particular, we analysed the key role of TF involved in interferon (IFN) response. We found that several TF could be induced by the IFN antiviral response, specifically some induced by IFN-stimulated gene factor 3 (ISGF3) and by unphosphorylated ISGF3, which were found to promote the transcription of several viral open reading frame. Moreover, we found 22 TF binding sites present only in the sequence of virus infecting humans but not bat coronavirus RaTG13. The 22 TF are involved in IFN, retinoic acid signalling and regulation of transcription by RNA polymerase II, thus facilitating its own replication cycle. This mechanism, by competition, may steal the human TF involved in these processes, explaining SARS-CoV-2's disruption of IFN-I signalling in host cells and the mechanism of the SARS retinoic acid depletion syndrome leading to the cytokine storm. We identified three TF binding sites present exclusively in the Brazilian SARS-CoV-2 P.1 variant that may explain the higher severity of the respiratory syndrome. These data shed light on SARS-CoV-2 dependence from the host transcription machinery associated with IFN response and strengthen our knowledge of the virus's transcription and replicative activity, thus paving the way for new targets for drug design and therapeutic approaches.

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