tetano
Editor, Senior Moderator
iScience
. 2023 Nov 13;26(12):108449.
doi: 10.1016/j.isci.2023.108449. eCollection 2023 Dec 15. Transcriptomic analysis of sorted lung cells revealed a proviral activity of the NF-κB pathway toward SARS-CoV-2
Anvita Bhargava[SUP] 1 [/SUP], Ugo Szachnowski[SUP] 2 [/SUP], Maxime Chazal[SUP] 1 [/SUP], Dominika Foretek[SUP] 1 2 [/SUP], Vincent Caval[SUP] 1 [/SUP], Sophie-Marie Aicher[SUP] 1 [/SUP], Juliana Pipoli da Fonseca[SUP] 3 [/SUP], Patricia Jeannin[SUP] 4 [/SUP], Guillaume Beauclair[SUP] 5 [/SUP], Marc Monot[SUP] 3 [/SUP], Antonin Morillon[SUP] 2 [/SUP], Nolwenn Jouvenet[SUP] 1 [/SUP]
Affiliations
Investigations of cellular responses to viral infection are commonly performed on mixed populations of infected and uninfected cells or using single-cell RNA sequencing, leading to inaccurate and low-resolution gene expression interpretations. Here, we performed deep polyA+ transcriptome analyses and novel RNA profiling of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infected lung epithelial cells, sorted based on the expression of the viral spike (S) protein. Infection caused a massive reduction in mRNAs and long non-coding RNAs (lncRNAs), including transcripts coding for antiviral factors, such as interferons (IFNs). This absence of IFN signaling probably explained the poor transcriptomic response of bystander cells co-cultured with S[SUP]+[/SUP] ones. NF-κB pathway and the inflammatory response escaped the global shutoff in S[SUP]+[/SUP] cells. Functional investigations revealed the proviral function of the NF-κB pathway and the antiviral activity of CYLD, a negative regulator of the pathway. Thus, our transcriptomic analysis on sorted cells revealed additional genes that modulate SARS-CoV-2 replication in lung cells.
Keywords: Cell; Transcriptomics; Virology.
. 2023 Nov 13;26(12):108449.
doi: 10.1016/j.isci.2023.108449. eCollection 2023 Dec 15. Transcriptomic analysis of sorted lung cells revealed a proviral activity of the NF-κB pathway toward SARS-CoV-2
Anvita Bhargava[SUP] 1 [/SUP], Ugo Szachnowski[SUP] 2 [/SUP], Maxime Chazal[SUP] 1 [/SUP], Dominika Foretek[SUP] 1 2 [/SUP], Vincent Caval[SUP] 1 [/SUP], Sophie-Marie Aicher[SUP] 1 [/SUP], Juliana Pipoli da Fonseca[SUP] 3 [/SUP], Patricia Jeannin[SUP] 4 [/SUP], Guillaume Beauclair[SUP] 5 [/SUP], Marc Monot[SUP] 3 [/SUP], Antonin Morillon[SUP] 2 [/SUP], Nolwenn Jouvenet[SUP] 1 [/SUP]
Affiliations
- PMID: 38213785
- PMCID: PMC10783605
- DOI: 10.1016/j.isci.2023.108449
Investigations of cellular responses to viral infection are commonly performed on mixed populations of infected and uninfected cells or using single-cell RNA sequencing, leading to inaccurate and low-resolution gene expression interpretations. Here, we performed deep polyA+ transcriptome analyses and novel RNA profiling of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infected lung epithelial cells, sorted based on the expression of the viral spike (S) protein. Infection caused a massive reduction in mRNAs and long non-coding RNAs (lncRNAs), including transcripts coding for antiviral factors, such as interferons (IFNs). This absence of IFN signaling probably explained the poor transcriptomic response of bystander cells co-cultured with S[SUP]+[/SUP] ones. NF-κB pathway and the inflammatory response escaped the global shutoff in S[SUP]+[/SUP] cells. Functional investigations revealed the proviral function of the NF-κB pathway and the antiviral activity of CYLD, a negative regulator of the pathway. Thus, our transcriptomic analysis on sorted cells revealed additional genes that modulate SARS-CoV-2 replication in lung cells.
Keywords: Cell; Transcriptomics; Virology.