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The variant gambit: COVID-19's next move.

ABSTRACT: More than a year after its emergence, COVID-19, the disease caused by SARS-CoV-2, continues to plague the world and dominate our daily lives. Even with the development of effective vaccines, this coronavirus pandemic continues to cause a fervor with the identification of major new variants hailing from the United Kingdom, South Africa, Brazil, and California. Coupled with worries over a distinct mink strain that has caused human infections and potential for further mutations, SARS-CoV-2 variants bring concerns for increased spread and escape from both vaccine and natural infection immunity. Here, we outline factors driving SARS-CoV-2 variant evolution, explore the potential impact of specific mutations, examine the risk of further mutations, and consider the experimental studies needed to understand the threat these variants pose. In this review, Plante et al. examine SARS-CoV-2 variants including B.1.1.7 (UK), B.1.351 (RSA), P.1 (Brazil), and B.1.429 (California). They focus on what factors contribute to variant emergence, mutations in and outside the spike protein, and studies needed to understand the impact of variants on infection, transmission, and vaccine efficacy.

SUBMITTER: Plante JA

PROVIDER: S-EPMC7919536 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Purpose: The goals of this study are to compare NGS-derived transcriptome profiling (RNA-seq) of COVID-19 kidney to normal controls Methods/Results: Kidney mRNA profile of human COVID-19 tissue was generated by deep sequencing using Illumina Novaseq6000 Paired-end 150. After filtering reads mapped to contamination database, the reads that were uniquely aligned to the exon and splicing-junction segments with a maximal 2 mismatches for each transcript were then counted as expression level for corresponding transcript. Next, RNA-seq reads count data were downloaded from public resource GTEx project (https://www.gtexportal.org/home/datasets) and 12 normal kidney tissue samples were extracted as controls. The differential analysis by fold change difference was carried out to identify dysregulated genes at 1.5 fold change. The differential expressed genes were then subjected to Gene Ontology function and Pathway (KEGG, Ingenuity IPA, BIOCARTA, NABA, Panther, PID, REACTOME, Wiki-pathway) enrichment analysis by Fisher-exact test. Conclusions: RNA sequencing data revealed that biological processes from upregulated genes were enriched for cell cycle, chromosome segregation, response to wounding, humoral immune response, and blood coagulation, suggesting that cell injury/regeneration, inflammatory response, and endothelial injury were the major disease processes involved. The biological processes from downregulated genes were enriched for ion transport, metabolic processes, and oxidation, likely secondary to severe tubular cell injury. Pathway analysis from both up- and downregulated genes showed enrichment of transmembrane transport, oxidation, and blood coagulation consistent with the GO terms analysis. Upregulated genes were enriched only for the FOXM1 pathway, which was recently reported to promote tubular cell proliferation during injury repair. Additionally, genes related to the renin-angiotensin system were downregulated, but ACE2 expression did not differ from normal controls.

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The variant gambit: COVID-19's next move.

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