Identifying key biomarkers and therapeutic candidates for post-COVID-19 depression through integrated omics and bioinformatics approaches DOI Creative Commons

Yi Zhou,

Chunhua Yang, Jing Zhou

et al.

Translational Neuroscience, Journal Year: 2024, Volume and Issue: 15(1)

Published: Jan. 1, 2024

Depression, the leading cause of disability worldwide, is known to be exacerbated by severe acute respiratory syndrome coronavirus 2 infection, worsening disease 2019 (COVID-19) outcomes. However, mechanisms and treatments for this comorbidity are not well understood. This study utilized Gene Expression Omnibus datasets COVID-19 depression, combined with protein-protein interaction networks, identify key genes. ontology Kyoto Encyclopedia Genes Genomes analyses were performed understand gene functions. The CIBERSORT algorithm NetworkAnalyst used examine relationship immune cell infiltration expression predict transcription factors (TFs) microRNAs (miRNAs) interactions. Connectivity Map database was drug interactions these TRUB1, PLEKHA7, FABP6 identified as genes enriched in pathways related function signaling. Seven TFs nineteen miRNAs found interact Nineteen drugs, including atorvastatin paroxetine, predicted significantly associated potential therapeutic agents depression. research provides new insights into molecular post-COVID-19 depression suggests strategies, marking a step forward understanding treating complex comorbidity.

Language: Английский

Enhanced complement activation and MAC formation accelerates severe COVID-19 DOI Creative Commons
Calder Ellsworth, Zhen Chen, Mark Xiao

et al.

Cellular and Molecular Life Sciences, Journal Year: 2024, Volume and Issue: 81(1)

Published: Sept. 16, 2024

Emerging evidence indicates that activation of complement system leading to the formation membrane attack complex (MAC) plays a detrimental role in COVID-19. However, their pathogenic roles have never been experimentally investigated before. We used three knock out mice strains (1. C3

Language: Английский

Citations

4
The picture theory of seven pathways associated with COVID-19 in the real world DOI Creative Commons
Jong‐Hoon Lee, Consolato Sergi, Richard E. Kast

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: April 8, 2024

Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces immune-mediated diseases. Interactions between the host and virus govern induction, resulting in multiorgan impacts. In 2021, as normal life was challenging during pandemic era, we analyzed SCI journals according to L. Wittgenstein's Tractatus Logi-co-Philosophicus. The pathophysiology of disease 2019 (COVID-19) involves following steps: 1) angiotensin-converting enzyme (ACE2) Toll-like receptor (TLR) pathways: 2) neuropilin (NRP) pathway, with seven papers continuing twenty-four: 3) sterile alpha motif (SAM) histidine-aspartate domain (HD)-containing protein 1 (SAMHD1) tetramerization two twelve: 4) inflammasome activation pathways, five thirteen: 5) cytosolic DNA sensor cyclic-GMP-AMP synthase (cGAS)/stimulator interferon genes (STING) (cGAS–STING) signaling six successful eleven: 6) spike fourteen twenty-three: 7) immunological memory engram thirteen successive eighteen: 8) excess acetylcholine three nine. We reconfirmed that COVID-19 (1-7) pathways a new pathway involving acetylcholine. Therefore, it is necessary therapeutically alleviate block pathological course harmoniously modulating innate lymphoid cells (ILCs) if diverse SARS-CoV-2 variants are subsequently encountered future.

Language: Английский

Citations

2
NSP6 inhibits the production of ACE2-containing exosomes to promote SARS-CoV-2 infectivity DOI Creative Commons
Xi Lv, Ran Chen,

Taizhen Liang

et al.

mBio, Journal Year: 2024, Volume and Issue: 15(3)

Published: Feb. 2, 2024

ABSTRACT The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has triggered a global pandemic, which severely endangers public health. Our and others’ works have shown that the angiotensin-converting enzyme (ACE2)-containing exosomes (ACE2-exos) superior antiviral efficacies, especially in response to emerging variants. However, mechanisms how virus counteracts host regulates ACE2-exos remain unclear. Here, we identified SARS-CoV-2 nonstructural protein 6 (NSP6) inhibits production by affecting level ACE2 as well tetraspanin-CD63 is key factor for exosome biogenesis. We further found stability CD63 maintained deubiquitination proteasome 26S subunit, non-ATPase 12 (PSMD12). NSP6 interacts with PSMD12 its function, consequently promoting degradation ACE2. As result, diminishes efficacy facilitates infect healthy bystander cells. Overall, our study provides valuable target discovery promising drugs treatment disease 2019. IMPORTANCE outbreak 2019 (COVID-19) vaccines antibodies declined rapid mutants. Angiotensin-converting 2-containing therapy exhibits broad neutralizing activity, could be used against various viral mutations. here revealed inhibited ACE2-exos, thereby infection adjacent identification new blocking depends on fully understanding virus-host interaction networks. sheds light mechanism resists defenses, would facilitate design ACE2-exos-based therapeutics COVID-19.

Language: Английский

Citations

1
The PDZ Domain of the E Protein in SARS-CoV Induces Carcinogenesis and Poor Prognosis in LUAD DOI
Shun Li,

Jinxuan Wang,

Xiaozhen Dai

et al.

Microbes and Infection, Journal Year: 2024, Volume and Issue: unknown, P. 105381 - 105381

Published: June 1, 2024

Language: Английский

Citations

1
The picture theory of seven pathways associated with COVID-19 in the real world DOI Creative Commons
Jong‐Hoon Lee, Consolato Sergi, Richard E. Kast

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Jan. 12, 2024

Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces immune-mediated diseases. Interactions between the host and virus govern induction, resulting in multiorgan impacts In 2021, as normal life was challenging during pandemic era, we analyzed SCI journals according to L. Wittgenstein's Tractatus Logi-co-Philosophicus. The pathophysiology of disease 2019 (COVID-19) involves 1) angiotensin-converting enzyme (ACE2) Toll-like receptor (TLR) pathways starting with eight, from 2022.01.14., rediscovered nineteen, 2024.01.10., 2) neuropilin (NRP) pathway seven successful twenty four, 3) sterile alpha motif (SAM) histidine-aspartate domain (HD)-containing protein 1 (SAMHD1) tetramerization two thirteen, 4) inflammasome activation five 5) cytosolic DNA sensor cyclic-GMP-AMP synthase (cGAS)/stimulator interferon genes (STING) (cGAS–STING) signaling six eleven, 6) spike fourteen three, 7) immunological memory engram thirteen eighteen, 8) excess acetylcholine three nine. We reconfirmed that COVID-19 involved (1–7) a new involving acetylcholine. Therefore, it is necessary therapeutically alleviate block pathological course harmoniously modulating innate lymphoid cells (ILCs) if subsequent diverse SARS-CoV-2 variants are encountered future.

Language: Английский

Citations

0
Identifying key biomarkers and therapeutic candidates for post-COVID-19 depression through integrated omics and bioinformatics approaches DOI Creative Commons

Yi Zhou,

Chunhua Yang, Jing Zhou

et al.

Translational Neuroscience, Journal Year: 2024, Volume and Issue: 15(1)

Published: Jan. 1, 2024

Depression, the leading cause of disability worldwide, is known to be exacerbated by severe acute respiratory syndrome coronavirus 2 infection, worsening disease 2019 (COVID-19) outcomes. However, mechanisms and treatments for this comorbidity are not well understood. This study utilized Gene Expression Omnibus datasets COVID-19 depression, combined with protein-protein interaction networks, identify key genes. ontology Kyoto Encyclopedia Genes Genomes analyses were performed understand gene functions. The CIBERSORT algorithm NetworkAnalyst used examine relationship immune cell infiltration expression predict transcription factors (TFs) microRNAs (miRNAs) interactions. Connectivity Map database was drug interactions these TRUB1, PLEKHA7, FABP6 identified as genes enriched in pathways related function signaling. Seven TFs nineteen miRNAs found interact Nineteen drugs, including atorvastatin paroxetine, predicted significantly associated potential therapeutic agents depression. research provides new insights into molecular post-COVID-19 depression suggests strategies, marking a step forward understanding treating complex comorbidity.

Language: Английский

Citations

0