ArticleVirus evolution2022
SARS-CoV-2 intra-host single-nucleotide variants associated with disease severity.
Article in Virus evolution, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- A graph homomorphism approach for unraveling histories of metastatic cancers and viral outbreaks under evolutionary constraints.Nature communications · 2025Article
- Diverse patterns of intra-host genetic diversity in chronically infected SARS-CoV-2 patients.Virus evolution · 2025Article
- Multi-Organ Spread and Intra-Host Diversity of SARS-CoV-2 Support Viral Persistence, Adaptation, and a Mechanism That Increases Evolvability.Journal of medical virology · 2024Article
- Refining SARS-CoV-2 intra-host variation by leveraging large-scale sequencing data.NAR genomics and bioinformatics · 2024Article
- Sequence signatures within the genome of SARS-CoV-2 can be used to predict host source.Microbiology spectrum · 2024Article
- Integrating artificial intelligence-based epitope prediction in a SARS-CoV-2 antibody discovery pipeline: caution is warranted.EBioMedicine · 2024Article
- Within-host genetic diversity of SARS-CoV-2 lineages in unvaccinated and vaccinated individuals.Nature communications · 2023Article
Corrections and comments
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Authors and funding
19 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Variants of severe acute respiratory syndrome coronavirus 2 frequently arise within infected individuals. Here, we explored the level and pattern of intra-host viral diversity in association with disease severity. Then, we analyzed information underlying these nucleotide changes to infer the impetus including mutational signatures and immune selection from neutralizing antibody or T-cell recognition. From 23 January to 31 March 2020, a set of cross-sectional samples were collected from individuals with homogeneous founder virus regardless of disease severity. Intra-host single-nucleotide variants (iSNVs) were enumerated using deep sequencing. Human leukocyte antigen (HLA) alleles were genotyped by Sanger sequencing. Medical records were collected and reviewed by attending physicians. A total of 836 iSNVs (3-106 per sample) were identified and distributed in a highly individualized pattern. The number of iSNVs paced with infection duration peaked within days and declined thereafter. These iSNVs did not stochastically arise due to a strong bias toward C > U/G > A and U > C/A > G substitutions in reciprocal proportion with escalating disease severity. Eight nonsynonymous iSNVs in the receptor-binding domain could escape from neutralization, and eighteen iSNVs were significantly associated with specific HLA alleles. The level and pattern of iSNVs reflect the
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.