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MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ORF3a (1)

ProteinS1 (1)

ProteinS (1)


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    T cell assays differentiate clinical and subclinical SARS-CoV-2 infection MESHDs from cross-reactive antiviral responses

    Authors: Ane Ogbe; Barbara Kronsteiner; Donal T Skelly; Matthew Pace; Anthony Brown; Emily Adland; Kareena Adair; Hossain Delowar Akhter; Mohammad Ali; Serat-E Ali; Adrienn Angyal; M. Azim Ansari; Carolina V Arancibia-Carcamo; Helen Brown; Senthil Chinnakannan; Christopher P Conlon; Catherine de Lara; Thushan de Silva; Christina Dold; Tao Dong Dong; Timothy Donnison; David W Eyre; Amy Flaxman; Helen A Fletcher; Joshua Gardner; James T Grist; Carl-Philipp Hackstein; Kanoot Jaruthamsophon; Katie Jeffrey; Teresa Lambe; Lian Lee; Wenqin Li; Nicholas Lim; Philippa C Matthews; Alexander J Mentzer; Shona C Moore; Dean J Naisbitt; Monday Ogese; Graham Ogg; Peter Openshaw; Munir Pirmohamed; Andrew J Pollard; Narayan Ramamurthy; Patpong Rongkard; Sarah Rowland-Jones; Oliver L Sampson; Gavin Screaton; Alessandro Sette; Lizzie Stafford; Craig Thompson; Paul J Thomson; Ryan Thwaites; Vinicius Vieira; Daniela Weiskopf; Panagiota Zacharopoulou; - Oxford Immunology Network Covid-19 Response T cell Consortium; - Oxford Protective T cell Immunology for COVID-19 (OPTIC) Clinical team; Lance Turtle; Paul Klenerman; Philip Goulder; John Frater; Eleanor Barnes; Susanna Dunachie

    doi:10.1101/2020.09.28.20202929 Date: 2020-09-29 Source: medRxiv

    A major issue in identification of protective T cell responses against SARS-CoV-2 lies in distinguishing people infected with SARS-CoV-2 from those with cross-reactive immunity generated by exposure to other coronaviruses. We characterised SARS-CoV-2 T cell immune responses in 168 PCR-confirmed SARS-CoV-2 infected MESHD subjects and 118 seronegative subjects without known SARS-CoV-2 exposure using a range of T cell assays that differentially capture immune cell function. Strong ex vivo ELISpot and proliferation responses to multiple antigens (including M, NP and ORF3 HGNC) were found in those who had been infected by SARS-CoV-2 but were rare in pre-pandemic and unexposed seronegative subjects. However, seronegative doctors with high occupational exposure and recent COVID-19 MESHD compatible illness showed patterns of T cell responses characteristic of infection, indicating that these readouts are highly sensitive. By contrast, over 90% of convalescent or unexposed people showed proliferation and cellular lactate responses to spike subunits S1 PROTEIN/S2, indicating pre-existing cross-reactive T cell populations. The detection of T cell responses to SARS-CoV-2 is therefore critically dependent on the choice of assay and antigen. Memory responses to specific non- spike proteins PROTEIN provides a method to distinguish recent infection from pre-existing immunity in exposed populations.

    A putative new SARS-CoV protein, 3a*, encoded in an ORF overlapping ORF3a PROTEIN ORF3a HGNC

    Authors: Andrew E Firth

    doi:10.1101/2020.05.12.088088 Date: 2020-05-12 Source: bioRxiv

    Identification of the full complement of genes in SARS-CoV-2 is a crucial step towards gaining a fuller understanding of its molecular biology. However, short and/or overlapping genes can be difficult to detect using conventional computational approaches, whereas high throughput experimental approaches - such as ribosome profiling - cannot distinguish translation of functional peptides from regulatory translation or translational noise. By studying regions showing enhanced conservation at synonymous sites in alignments of SARS-CoV MESHD and related viruses (subgenus Sarbecovirus), and correlating with the conserved presence of an open reading frame and plausible translation mechanism, we identified a putative new gene, ORF3a PROTEIN*, overlapping ORF3a PROTEIN in an alternative reading frame. A recently published ribosome profiling study confirmed that ORF3a PROTEIN* is indeed translated during infection. ORF3a PROTEIN* is conserved across the subgenus Sarbecovirus, and encodes a 40-41 amino acid predicted transmembrane protein.

    The origin and underlying driving forces of the SARS-CoV-2 outbreak

    Authors: Shu-Miaw Chaw; Jui-Hung Tai; Shi-Lun Chen; Chia-Hung Hsieh; Sui-Yuan Chang; Shiou-Hwei Yeh; Wei-Shiung Yang; Pei-Jer Chen; Hurng-Yi Wang

    doi:10.1101/2020.04.12.038554 Date: 2020-04-14 Source: bioRxiv

    The spread of SARS-CoV-2 since December 2019 has become a pandemic and impacted many aspects of human society. Here, we analyzed genetic variation of SARS-CoV-2 and its related coronavirus and found the evidence of intergenomic recombination. After correction for mutational bias, analysis of 137 SARS-CoV-2 genomes as of 2/23/2020 revealed the excess of low frequency mutations on both synonymous and nonsynonymous sites which is consistent with recent origin of the virus. In contrast to adaptive evolution previously reported for SARS-CoV MESHD in its brief epidemic in 2003, our analysis of SARS-CoV-2 genomes shows signs of relaxation of selection. The sequence similarity of the spike receptor binding domain between SARS-CoV-2 and a sequence from pangolin is probably due to an ancient intergenomic introgression. Therefore, SARS-CoV-2 might have cryptically circulated within humans for years before being recently noticed. Data from the early outbreak and hospital archives are needed to trace its evolutionary path and reveal critical steps required for effective spreading. Two mutations, 84S in orf8 protein and 251V in orf3 HGNC protein, occurred coincidentally with human intervention. The 84S first appeared on 1/5/2020 and reached a plateau around 1/23/2020, the lockdown of Wuhan. 251V emerged on 1/21/2020 and rapidly increased its frequency. Thus, the roles of these mutations on infectivity need to be elucidated. Genetic diversity of SARS-CoV-2 collected from China was two time higher than those derived from the rest of the world. In addition, in network analysis, haplotypes collected from Wuhan city were at interior and have more mutational connections, both of which are consistent with the observation that the outbreak of cov-19 was originated from China. SUMMARYIn contrast to adaptive evolution previously reported for SARS-CoV in its brief epidemic, our analysis of SARS-CoV-2 genomes shows signs of relaxation of selection. The sequence similarity of the spike receptor binding domain between SARS-CoV-2 and a sequence from pangolin is probably due to an ancient intergenomic introgression. Therefore, SARS-CoV-2 might have cryptically circulated within humans for years before being recently noticed. Data from the early outbreak and hospital archives are needed to trace its evolutionary path and reveal critical steps required for effective spreading. Two mutations, 84S in orf8 protein and 251V in orf3 HGNC protein, occurred coincidentally with human intervention. The 84S first appeared on 1/5/2020 and reached a plateau around 1/23/2020, the lockdown of Wuhan. 251V emerged on 1/21/2020 and rapidly increased its frequency. Thus, the roles of these mutations on infectivity need to be elucidated.

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