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      Expansion of a SARS-CoV-2 Delta variant with an 872 nt deletion encompassing ORF7a, ORF7b and ORF8, Poland, July to August 2021

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          Abstract

          Routine genomic surveillance on samples from COVID-19 patients collected in Poland during summer 2021 revealed the emergence of a SARS-CoV-2 Delta variant with a large 872 nt deletion. This change, confirmed by Sanger and deep sequencing, causes complete loss of ORF7a, ORF7b, and ORF8 genes. The index case carrying the deletion is unknown. The standard pipeline for sequencing may mask this deletion with a long stretch of N’s. Effects of this deletion on phenotype or immune evasion needs further study.

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          Effects of a major deletion in the SARS-CoV-2 genome on the severity of infection and the inflammatory response: an observational cohort study

          Barnaby E Young, Siew-Wai Fong, Yi-Hao Chan … (2020)
          Summary Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants with a 382-nucleotide deletion (∆382) in the open reading frame 8 (ORF8) region of the genome have been detected in Singapore and other countries. We investigated the effect of this deletion on the clinical features of infection. Methods We retrospectively identified patients who had been screened for the ∆382 variant and recruited to the PROTECT study—a prospective observational cohort study conducted at seven public hospitals in Singapore. We collected clinical, laboratory, and radiological data from patients' electronic medical records and serial blood and respiratory samples taken during hospitalisation and after discharge. Individuals infected with the ∆382 variant were compared with those infected with wild-type SARS-CoV-2. Exact logistic regression was used to examine the association between the infection groups and the development of hypoxia requiring supplemental oxygen (an indicator of severe COVID-19, the primary endpoint). Follow-up for the study's primary endpoint is completed. Findings Between Jan 22 and March 21, 2020, 278 patients with PCR-confirmed SARS-CoV-2 infection were screened for the ∆382 deletion and 131 were enrolled onto the study, of whom 92 (70%) were infected with the wild-type virus, ten (8%) had a mix of wild-type and ∆382-variant viruses, and 29 (22%) had only the ∆382 variant. Development of hypoxia requiring supplemental oxygen was less frequent in the ∆382 variant group (0 [0%] of 29 patients) than in the wild-type only group (26 [28%] of 92; absolute difference 28% [95% CI 14–28]). After adjusting for age and presence of comorbidities, infection with the ∆382 variant only was associated with lower odds of developing hypoxia requiring supplemental oxygen (adjusted odds ratio 0·07 [95% CI 0·00–0·48]) compared with infection with wild-type virus only. Interpretation The ∆382 variant of SARS-CoV-2 seems to be associated with a milder infection. The observed clinical effects of deletions in ORF8 could have implications for the development of treatments and vaccines. Funding National Medical Research Council Singapore.
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            The ORF6, ORF8 and nucleocapsid proteins of SARS-CoV-2 inhibit type I interferon signaling pathway

            Jin-Yan Li, Ce-Heng Liao, Qiong Wang … (2020)
            Highlights • We firstly screened the viral proteins of SARS-CoV-2 by luciferase reporter gene assay and found that the viral ORF6, ORF8 and nucleocapsid proteins showed strong inhibition on type I interferon (IFN-β), NF-κB-responsive and ISRE promoter after infection with Sendai virus. • ORF6 and ORF8, but not nucleocapsid proteins, were able to inhibit the ISRE promoter after treatment with interferon beta, indicating that they play a role in different nodes and may have different mechanisms to regulate host interferon pathway. • ORF6, ORF8, and nucleocapsid proteins of SARS-CoV-2 significantly suppressed SeV-induced mRNA expression of IFN-β and ISG gene including ISG56 and ISG54. • We identified ORF6, ORF8, and nucleocapsid proteins of SARS-CoV-2 as type I IFN antagonists.
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              Temporal signal and the phylodynamic threshold of SARS-CoV-2

              Sebastian Duchêne, Leo Featherstone, Melina Haritopoulou-Sinanidou … (2020)
              Abstract The ongoing SARS-CoV-2 outbreak marks the first time that large amounts of genome sequence data have been generated and made publicly available in near real-time. Early analyses of these data revealed low sequence variation, a finding that is consistent with a recently emerging outbreak, but which raises the question of whether such data are sufficiently informative for phylogenetic inferences of evolutionary rates and time scales. The phylodynamic threshold is a key concept that refers to the point in time at which sufficient molecular evolutionary change has accumulated in available genome samples to obtain robust phylodynamic estimates. For example, before the phylodynamic threshold is reached, genomic variation is so low that even large amounts of genome sequences may be insufficient to estimate the virus’s evolutionary rate and the time scale of an outbreak. We collected genome sequences of SARS-CoV-2 from public databases at 8 different points in time and conducted a range of tests of temporal signal to determine if and when the phylodynamic threshold was reached, and the range of inferences that could be reliably drawn from these data. Our results indicate that by February 2nd 2020, estimates of evolutionary rates and time scales had become possible. Analyses of subsequent data sets, that included between 47 to 122 genomes, converged at an evolutionary rate of about 1.1 × 10−3 subs/site/year and a time of origin of around late November 2019. Our study provides guidelines to assess the phylodynamic threshold and demonstrates that establishing this threshold constitutes a fundamental step for understanding the power and limitations of early data in outbreak genome surveillance.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Euro Surveill
                Journal ID (iso-abbrev): Euro Surveill
                Journal ID (publisher-id): eurosurveillance
                Title: Eurosurveillance
                Publisher: European Centre for Disease Prevention and Control (ECDC)
                ISSN (Print): 1025-496X
                ISSN (Electronic): 1560-7917
                Publication date (Print): 30 September 2021
                Volume: 26
                Issue: 39
                Electronic Location Identifier: 2100902
                Affiliations
                [1 ]Virogenetics Laboratory of Virology, Malopolska Centre of Biotechnology, Jagiellonian University, Krakow, Poland
                [2 ]Laboratory of Recombinant Vaccines, Intercollegiate Faculty of Biotechnology of University of Gdansk and Medical University of Gdansk, Gdansk, Poland
                [3 ]Human Genome Research Variation Group, Malopolska Centre of Biotechnology, Jagiellonian University, Krakow, Poland
                [4 ]genXone SA, Research & Development Laboratory, Suchy Las, Poland
                [5 ]Bioinformatics Research Group, Malopolska Centre of Biotechnology, Jagiellonian University, Krakow, Poland
                [6 ]Diagnostyka Medical Laboratories, Krakow, Poland
                [7 ]Laboratory of Virus Molecular Biology, Intercollegiate Faculty of Biotechnology of University of Gdansk and Medical University of Gdansk, Gdansk, Poland
                [8 ]Department of Tropical Parasitology, Institute of Maritime and Tropical Medicine, Medical University of Gdansk, Gdynia, Poland
                Author notes
                [*]

                These authors contributed equally to this article and share first authorship

                Correspondence: Krzysztof Pyrc ( k.a.pyrc@ 123456uj.edu.pl )

                Author information
                http://orcid.org/0000-0002-3867-7688
                Article
                Publisher ID: 2100902 Publisher ID: 2100902
                DOI: 10.2807/1560-7917.ES.2021.26.39.2100902
                PMC ID: 8485581
                PubMed ID: 34596017
                SO-VID: d8443b49-c482-4c4f-aefc-7e06518e3527
                Copyright © This article is copyright of the authors or their affiliated institutions, 2021.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY 4.0) Licence. You may share and adapt the material, but must give appropriate credit to the source, provide a link to the licence, and indicate if changes were made.

                History
                Date received : 16 September 2021
                Date accepted : 30 September 2021
                Categories
                Subject: Rapid Communication
                Custom metadata
                sequence 2

                Keywords: sars-cov-2,variant,deletion,pandemic,detection
                Data availability:
                Keywords: sars-cov-2, variant, deletion, pandemic, detection

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