Longitudinal host transcriptional responses to SARS-CoV-2 infection in adults with extremely high viral load.

Longitudinal host transcriptional responses to SARS-CoV-2 infection in adults with extremely high viral load.

Publication date: Jan 17, 2025

Current understanding of viral dynamics of SARS-CoV-2 and host responses driving the pathogenic mechanisms in COVID-19 is rapidly evolving. Here, we conducted a longitudinal study to investigate gene expression patterns during acute SARS-CoV-2 illness. Cases included SARS-CoV-2 infected individuals with extremely high viral loads early in their illness, individuals having low SARS-CoV-2 viral loads early in their infection, and individuals testing negative for SARS-CoV-2. We could identify widespread transcriptional host responses to SARS-CoV-2 infection that were initially most strongly manifested in patients with extremely high initial viral loads, then attenuating within the patient over time as viral loads decreased. Genes correlated with SARS-CoV-2 viral load over time were similarly differentially expressed across independent datasets of SARS-CoV-2 infected lung and upper airway cells, from both in vitro systems and patient samples. We also generated expression data on the human nose organoid model during SARS-CoV-2 infection. The human nose organoid-generated host transcriptional response captured many aspects of responses observed in the above patient samples, while suggesting the existence of distinct host responses to SARS-CoV-2 depending on the cellular context, involving both epithelial and cellular immune responses. Our findings provide a catalog of SARS-CoV-2 host response genes changing over time and magnitude of these host responses were significantly correlated to viral load.

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Concepts Keywords
Covid Adult
Driving COVID-19
Low Female
Pathogenic Host-Pathogen Interactions
Viral Humans
Longitudinal Studies
Lung
Male
SARS-CoV-2
Viral Load

Semantics

Type Source Name
disease IDO host
disease MESH SARS-CoV-2 infection
pathway REACTOME SARS-CoV-2 Infection
disease MESH viral load
disease MESH infection
disease IDO history
disease IDO process
pathway REACTOME Reproduction
disease MESH asymptomatic infection
disease MESH death
disease MESH obesity
disease MESH cardiovascular disease
disease IDO replication
disease MESH viral shedding
pathway KEGG Viral replication
pathway REACTOME Apoptosis
pathway KEGG p53 signaling pathway
disease MESH complications
disease IDO pathogen

Original Article

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