Atlas of interactions between SARS-CoV-2 macromolecules and host proteins

Li, Guangnan; Tang, Zhidong; Fan, Weiliang; Wang, Xi; Huang, Li; Jia, Yu; Wang, Manli; Hú, Zhìhóng; Zhou, Yu

doi:10.1016/j.cellin.2022.100068

Cited by 13 publications

(7 citation statements)

References 90 publications

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“…(Proteins identified in that study are not listed in Table 2 in order to keep it within manageable proportions.) This may be contrasted with other studies that identified FANCI interacting with Nsp3 and 7, M protein and ORF7a [158,181,183]. This was also the case for BRCA1, BRCA2, ERCC5, ERCC6L, XRCC5 and XRCC6, where a large number of associated SARS-CoV-2 proteins were identified for each [179].…”

Section: Association Of Sars-cov-2 Proteins With Ddr Componentscontrasting

confidence: 84%

“…There have been several large-scale studies to identify the SARS-CoV-2 interactome, based on co-immunoprecipitation, yeast 2 hybrid and biotin-streptavidin based-protocols (see, for example, [158,[176][177][178][179][180][181][182][183][184]); in some cases, published data have been consolidated into a resource summarizing reported interactions (for example, [185]). There are appreciable variations in the binding proteins reported in the different studies but similar major groups of proteins from specific cellular pathways have been identified as significant targets for the virus.…”

Section: Association Of Sars-cov-2 Proteins With Ddr Componentsmentioning

confidence: 99%

“…Role in DNA replication [158] ZC3H18 Binds the cap-binding complex on capped RNAs [176,180] Membrane (M) protein FANCI Fanconi anaemia component I. Role in DSB repair and repair of inter-strand crosslinks [176,183] Ligase 3 Binds to XRCC1 and is involved in base excision repair [180] Timeless Involved in replication stress and genome stability [165] RINT1 RAD50 interactor 1. Regulates cell cycle and telomere length [158] Nucleocapsid (N) protein hnRNPUL2 RNA-binding protein involved in homologous recombination with the MRN complex [181] ERCC6L Excision repair 6-like protein, a DNA translocase involved in the mitotic spindle [158] RAD23B A role in nucleotide excision repair of bulky lesions and oxidative DNA damage [184] Spike (S) protein RINT1 RAD50 interactor 1.…”

Section: Sars-cov-2 Protein Associated Cellular Ddr Protein Ddr Prote...mentioning

confidence: 99%

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SARS-CoV-2 and the DNA damage response

Grand

2023

Journal of General Virology

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The recent coronavirus disease 2019 (COVID-19) pandemic was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is characterized by respiratory distress, multiorgan dysfunction and, in some cases, death. The virus is also responsible for post-COVID-19 condition (commonly referred to as ‘long COVID’). SARS-CoV-2 is a single-stranded, positive-sense RNA virus with a genome of approximately 30 kb, which encodes 26 proteins. It has been reported to affect multiple pathways in infected cells, resulting, in many cases, in the induction of a ‘cytokine storm’ and cellular senescence. Perhaps because it is an RNA virus, replicating largely in the cytoplasm, the effect of SARS-Cov-2 on genome stability and DNA damage responses (DDRs) has received relatively little attention. However, it is now becoming clear that the virus causes damage to cellular DNA, as shown by the presence of micronuclei, DNA repair foci and increased comet tails in infected cells. This review considers recent evidence indicating how SARS-CoV-2 causes genome instability, deregulates the cell cycle and targets specific components of DDR pathways. The significance of the virus’s ability to cause cellular senescence is also considered, as are the implications of genome instability for patients suffering from long COVID.

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Section: Association Of Sars-cov-2 Proteins With Ddr Componentscontrasting

confidence: 84%

Section: Association Of Sars-cov-2 Proteins With Ddr Componentsmentioning

confidence: 99%

Section: Sars-cov-2 Protein Associated Cellular Ddr Protein Ddr Prote...mentioning

confidence: 99%

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SARS-CoV-2 and the DNA damage response

Grand

2023

Journal of General Virology

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“…The COVID-19 pandemic served as a wake-up call to human awareness regarding the threat of the newly emerging coronaviruses to humans ( Li et al., 2023 ). MERS-CoV, which has the highest reported case fatality rate of 36%, continues to transmit sporadically in the Middle East, raising concerns about the potential for future pandemics caused by MERS-CoV-related viruses ( WHO, 2012 ).…”

Section: Perspectivesmentioning

confidence: 99%

ACE2-using merbecoviruses: Further evidence of convergent evolution of ACE2 recognition by NeoCoV and other MERS-CoV related viruses

Xiong,

Ma,

Liu

et al. 2024

Cell Insight

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“…Although rapid induction of type I IFNs limits virus propagation, a sustained increase in the levels of type I IFNs in the late phase of infection is associated with aberrant inflammation and poor clinical outcomes. It has been suggested that in patients with COVID-19, the cGAS-MITA/STING pathway is critical to the type I IFN immunopathology of extrapulmonary complications in lung endothelial cells after mtDNA release [ 11 , 154 , 155 ]. There is accumulating evidence showing that mtDNA sensing by the cGAS-MITA/STING pathway plays a critical role in antiviral host defense, but how viral infection triggers Ca 2+ import into mitochondria via MCU to induce mitostress and how MPTP-VDAC oligomer-mediated mtDNA release is regulated after viral infection are not fully understood.…”

Section: Physiological and Pathological Effects Of Mtdna Releasementioning

confidence: 99%

Mitochondrial DNA-triggered innate immune response: mechanisms and diseases

Hu,

Shu

2023

Cell Mol Immunol

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Various cellular stress conditions trigger mitochondrial DNA (mtDNA) release from mitochondria into the cytosol. The released mtDNA is sensed by the cGAS-MITA/STING pathway, resulting in the induced expression of type I interferon and other effector genes. These processes contribute to the innate immune response to viral infection and other stress factors. The deregulation of these processes causes autoimmune diseases, inflammatory metabolic disorders and cancer. Therefore, the cGAS-MITA/STING pathway is a potential target for intervention in infectious, inflammatory and autoimmune diseases as well as cancer. In this review, we focus on the mechanisms underlying the mtDNA-triggered activation of the cGAS-MITA/STING pathway, the effects of the pathway under various physiological and pathological conditions, and advances in the development of drugs that target cGAS and MITA/STING.

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Atlas of interactions between SARS-CoV-2 macromolecules and host proteins

Cited by 13 publications

References 90 publications

SARS-CoV-2 and the DNA damage response

SARS-CoV-2 and the DNA damage response

ACE2-using merbecoviruses: Further evidence of convergent evolution of ACE2 recognition by NeoCoV and other MERS-CoV related viruses

Mitochondrial DNA-triggered innate immune response: mechanisms and diseases

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