tetano
Editor, Senior Moderator
Commun Biol
. 2021 May 17;4(1):590.
doi: 10.1038/s42003-021-02095-0.
Genome-wide bioinformatic analyses predict key host and viral factors in SARS-CoV-2 pathogenesis
Mariana G Ferrarini[SUP] #[/SUP][SUP] 1 [/SUP], Avantika Lal[SUP] #[/SUP][SUP] 2 [/SUP], Rita Rebollo[SUP] 1 [/SUP], Andreas J Gruber[SUP] 3 [/SUP], Andrea Guarracino[SUP] 4 [/SUP], Itziar Martinez Gonzalez[SUP] 5 [/SUP], Taylor Floyd[SUP] 6 [/SUP], Daniel Siqueira de Oliveira[SUP] 7 [/SUP], Justin Shanklin[SUP] 8 [/SUP], Ethan Beausoleil[SUP] 8 [/SUP], Taneli Pusa[SUP] 9 [/SUP], Brett E Pickett[SUP] 10 [/SUP], Vanessa Aguiar-Pulido[SUP] 11 [/SUP]
Affiliations
Abstract
The novel betacoronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused a worldwide pandemic (COVID-19) after emerging in Wuhan, China. Here we analyzed public host and viral RNA sequencing data to better understand how SARS-CoV-2 interacts with human respiratory cells. We identified genes, isoforms and transposable element families that are specifically altered in SARS-CoV-2-infected respiratory cells. Well-known immunoregulatory genes including CSF2, IL32, IL-6 and SERPINA3 were differentially expressed, while immunoregulatory transposable element families were upregulated. We predicted conserved interactions between the SARS-CoV-2 genome and human RNA-binding proteins such as the heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) and eukaryotic initiation factor 4 (eIF4b). We also identified a viral sequence variant with a statistically significant skew associated with age of infection, that may contribute to intracellular host-pathogen interactions. These findings can help identify host mechanisms that can be targeted by prophylactics and/or therapeutics to reduce the severity of COVID-19.
. 2021 May 17;4(1):590.
doi: 10.1038/s42003-021-02095-0.
Genome-wide bioinformatic analyses predict key host and viral factors in SARS-CoV-2 pathogenesis
Mariana G Ferrarini[SUP] #[/SUP][SUP] 1 [/SUP], Avantika Lal[SUP] #[/SUP][SUP] 2 [/SUP], Rita Rebollo[SUP] 1 [/SUP], Andreas J Gruber[SUP] 3 [/SUP], Andrea Guarracino[SUP] 4 [/SUP], Itziar Martinez Gonzalez[SUP] 5 [/SUP], Taylor Floyd[SUP] 6 [/SUP], Daniel Siqueira de Oliveira[SUP] 7 [/SUP], Justin Shanklin[SUP] 8 [/SUP], Ethan Beausoleil[SUP] 8 [/SUP], Taneli Pusa[SUP] 9 [/SUP], Brett E Pickett[SUP] 10 [/SUP], Vanessa Aguiar-Pulido[SUP] 11 [/SUP]
Affiliations
- PMID: 34002013
- DOI: 10.1038/s42003-021-02095-0
Abstract
The novel betacoronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused a worldwide pandemic (COVID-19) after emerging in Wuhan, China. Here we analyzed public host and viral RNA sequencing data to better understand how SARS-CoV-2 interacts with human respiratory cells. We identified genes, isoforms and transposable element families that are specifically altered in SARS-CoV-2-infected respiratory cells. Well-known immunoregulatory genes including CSF2, IL32, IL-6 and SERPINA3 were differentially expressed, while immunoregulatory transposable element families were upregulated. We predicted conserved interactions between the SARS-CoV-2 genome and human RNA-binding proteins such as the heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) and eukaryotic initiation factor 4 (eIF4b). We also identified a viral sequence variant with a statistically significant skew associated with age of infection, that may contribute to intracellular host-pathogen interactions. These findings can help identify host mechanisms that can be targeted by prophylactics and/or therapeutics to reduce the severity of COVID-19.