ArticleScientific reports2018
Attenuation of replication by a 29 nucleotide deletion in SARS-coronavirus acquired during the early stages of human-to-human transmission.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.
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133 citing papers in PubMed, 1 synthesis or guideline pooled it, 226 citations in OpenAlex.
- Characterization of SARS-CoV-2 different variants and related morbidity and mortality: a systematic review.European journal of medical research · 2021Pooled it
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- SARS-CoV-2 ORF8 modulates lung inflammation and clinical disease progression.PLoS pathogens · 2024Article
- Properties and Mechanisms of Deletions, Insertions, and Substitutions in the Evolutionary History of SARS-CoV-2.International journal of molecular sciences · 2024Review
- Unraveling the genetic variations underlying virulence disparities among SARS-CoV-2 strains across global regions: insights from Pakistan.Virology journal · 2024Article
- SARS-CoV-2 and innate immunity: the good, the bad, and the "goldilocks".Cellular & molecular immunology · 2024Review
- Evolutionary deletions within the SARS-CoV-2 genome as signature trends for virus fitness and adaptation.Journal of virology · 2024Review
- Distinct phenotype of SARS-CoV-2 Omicron BA.1 in human primary cells but no increased host range in cell lines of putative mammalian reservoir species.Virus research · 2024Article
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- ORF3c is expressed in SARS-CoV-2-infected cells and inhibits innate sensing by targeting MAVS.EMBO reports · 2023Article
- The 29-nucleotide deletion in SARS-CoV: truncated versions of ORF8 are under purifying selection.BMC genomics · 2023Article
- The relevant information about the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) using the five-question approach (when, where, what, why, and how) and its impact on the environment.Environmental science and pollution research international · 2023Review
- ViReMa: a virus recombination mapper of next-generation sequencing data characterizes diverse recombinant viral nucleic acids.GigaScience · 2023Article
- Deletions across the SARS-CoV-2 Genome: Molecular Mechanisms and Putative Functional Consequences of Deletions in Accessory Genes.Microorganisms · 2023Article
- Unconventional secretion of unglycosylated ORF8 is critical for the cytokine storm during SARS-CoV-2 infection.PLoS pathogens · 2023Article
- The frequency of defective genomes in Omicron differs from that of the Alpha, Beta and Delta variants.Scientific reports · 2022Article
- Extensive Recombination-driven Coronavirus Diversification Expands the Pool of Potential Pandemic Pathogens.Genome biology and evolution · 2022Article
- Emergence and spreading of the largest SARS-CoV-2 deletion in the Delta AY.20 lineage from Uruguay.Gene reports · 2022Article
- "Mutation blacklist" and "mutation whitelist" of SARS-CoV-2.Journal of biosafety and biosecurity · 2022Article
73 more citing papers are in PubMed but not listed here.
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17 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A 29 nucleotide deletion in open reading frame 8 (ORF8) is the most obvious genetic change in severe acute respiratory syndrome coronavirus (SARS-CoV) during its emergence in humans. In spite of intense study, it remains unclear whether the deletion actually reflects adaptation to humans. Here we engineered full, partially deleted (-29 nt), and fully deleted ORF8 into a SARS-CoV infectious cDNA clone, strain Frankfurt-1. Replication of the resulting viruses was compared in primate cell cultures as well as Rhinolophus bat cells made permissive for SARS-CoV replication by lentiviral transduction of the human angiotensin-converting enzyme 2 receptor. Cells from cotton rat, goat, and sheep provided control scenarios that represent host systems in which SARS-CoV is neither endemic nor epidemic. Independent of the cell system, the truncation of ORF8 (29 nt deletion) decreased replication up to 23-fold. The effect was independent of the type I interferon response. The 29 nt deletion in SARS-CoV is a deleterious mutation acquired along the initial human-to-human transmission chain. The resulting loss of fitness may be due to a founder effect, which has rarely been documented in processes of viral emergence. These results have important implications for the retrospective assessment of the threat posed by SARS.
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