When cyclin‐dependent kinases meet viral infections, including SARS‐CoV‐2

Yan, Yan; Tang, Yan-Dong; Zheng, Chunfu

doi:10.1002/jmv.27719

Cited by 13 publications

(9 citation statements)

References 73 publications

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“…Further study is necessary to understand the interaction of OAS1 with CLIC1 and its function in IAV replication. CDK2 activates the viral DNA synthesis of herpes simplex virus 1 (HSV-1) and promotes HIV-1 and SARS-CoV-2 replication [ 39 , 40 ]. SARS-CoV-2 infection dysregulates CDK signaling pathways to arrest S/G2-like phase, creating favourable conditions for viral replication [ 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

Chloride Intracellular Channel Protein 1 (CLIC1) Is a Critical Host Cellular Factor for Influenza A Virus Replication

Rashid,

Coombs

2024

Viruses

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(1) Background: Influenza A Virus (IAV) uses host cellular proteins during replication in host cells. IAV infection causes elevated expression of chloride intracellular channel protein 1 (CLIC1) in lung epithelial cells, but the importance of this protein in IAV replication is unknown. (2) In this study, we determined the role of CLIC1 in IAV replication by investigating the effects of CLIC1 knockdown (KD) on IAV viral protein translation, genomic RNA transcription, and host cellular proteome dysregulation. (3) Results: CLIC1 KD in A549 human lung epithelial cells resulted in a significant decrease in progeny supernatant IAV, but virus protein expression was unaffected. However, a significantly larger number of viral RNAs accumulated in CLIC1 KD cells. Treatment with a CLIC1 inhibitor also caused a significant reduction in IAV replication, suggesting that CLIC1 is an important host factor in IAV replication. SomaScan®, which measures 1322 proteins, identified IAV-induced dysregulated proteins in wild-type cells and in CLIC1 KD cells. The expression of 116 and 150 proteins was significantly altered in wild-type and in CLIC1 KD cells, respectively. A large number of the dysregulated proteins in CLIC1 KD cells were associated with cellular transcription and predicted to be inhibited during IAV replication. (4) Conclusions: This study suggests that CLIC1 is involved in later stages of IAV replication. Further investigation should clarify mechanism(s) for the development of anti-IAV drugs targeting CLIC1 protein.

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Section: Discussionmentioning

confidence: 99%

Chloride Intracellular Channel Protein 1 (CLIC1) Is a Critical Host Cellular Factor for Influenza A Virus Replication

Rashid,

Coombs

2024

Viruses

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“…SAMHD1 has a target motif for cyclin-dependent kinase 1 (CDK1) ( 592 TPQK 595 : the CDK-targeted motif driving threonine 592 (T592) phosphorylation) 71 . CDKs are protein kinases that play key roles in cell division, transcriptional regulation, and viral infections 72 . SARS-CoV-2 infection triggers the redistribution of cyclin D1 and D3 from the nucleus to the cytoplasm and subsequent proteasomal degradation.…”

Section: The Samhd1 Tetramerization Pathwaymentioning

confidence: 99%

The picture theory of seven pathways associated with COVID-19 in the real world

Lee,

Sergi,

Kast

et al. 2024

Preprint

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

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“…SAMHD1 has a target motif for cyclin-dependent kinase 1 (CDK1) ( 592 TPQK 595 : the CDK-targeted motif driving threonine 592 (T592) phosphorylation) 70 . CDKs are protein kinases that play key roles in cell division, transcriptional regulation, and viral infections 71 . SARS-CoV-2 infection triggers and redistributes cyclin D1 and D3 from the nucleus to the cytoplasm and subsequent proteasomal degradation.…”

Section: The Samhd1 Tetramerization Pathwaymentioning

confidence: 99%

The picture theory of seven pathways associated with COVID-19 in the real world

Lee,

Sergi,

Kast

et al. 2024

Preprint

View full text Add to dashboard Cite

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

show abstract

When cyclin‐dependent kinases meet viral infections, including SARS‐CoV‐2

Cited by 13 publications

References 73 publications

Chloride Intracellular Channel Protein 1 (CLIC1) Is a Critical Host Cellular Factor for Influenza A Virus Replication

Chloride Intracellular Channel Protein 1 (CLIC1) Is a Critical Host Cellular Factor for Influenza A Virus Replication

The picture theory of seven pathways associated with COVID-19 in the real world

The picture theory of seven pathways associated with COVID-19 in the real world

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