Related references
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Summary: This study reveals that the viral protein ORF3a from SARS-CoV-2 can interact with STING and disrupt the STING-LC3 interaction, thereby inhibiting cGAS-STING-induced autophagy. This unique function of ORF3a facilitates viral replication. Furthermore, the study shows that activation of bat STING can induce autophagy and antiviral activity, but ORF3a from bat coronaviruses can block these functions. The ability of ORF3a to inhibit STING-induced autophagy appears to be an acquired function of SARS-CoV-2 ORF3a.
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Ming Zhao et al.
Summary: G3BP1 primes cGAS for prompt activation by engaging cGAS in a primary liquid-phase condensation state, leading to efficient liquid-liquid phase separation upon DNA challenge for rapid response.
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Sean M. Cascarina et al.
Summary: In response to the SARS-CoV-2 pandemic, labs worldwide have focused on studying the phase separation of viral proteins, particularly the N protein of SARS-CoV-2. This review discusses the potential functions of N protein phase separation in viral replication, RNA packaging, and host-cell response, and emphasizes the importance of comparing results across studies.
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Summary: This study reveals the mechanism behind aberrant type I interferon responses in COVID-19 through the cGAS-STING pathway and demonstrates its importance in severe cases. By using animal and lung-on-chip models, the study provides insights into host-directed therapeutic strategies for COVID-19.
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Mei Dang et al.
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Pharmacology & Pharmacy
Tiago J. Costa et al.
Summary: This study demonstrates that SARS-CoV-2 infection impairs mitochondrial function and activates TLR9 signaling in endothelial cells, leading to inflammatory responses and endothelial dysfunction. Targeting mitochondrial metabolic pathways may offer new therapeutic strategies for COVID-19.
VASCULAR PHARMACOLOGY
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Chao Shang et al.
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FRONTIERS IN MICROBIOLOGY
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Christopher J. Neufeldt et al.
Summary: SARS-CoV-2 infection can lead to severe symptoms and long-lasting lung damage or death. This is often associated with high levels of pro-inflammatory cytokines and low antiviral responses. A specific activation of NF-kappa B and block of IRF3 nuclear translocation were observed in infected cells. The inflammatory response is mediated by cGAS-STING activation and can be attenuated through STING-targeting drugs.
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Icaro Putinhon Caruso et al.
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Editorial Material
Immunology
Evangelos Andreakos
Summary: This study identifies the cGAS-STING pathway as a major driver of pathological type I interferon responses in COVID-19.
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Miriam Merad et al.
Summary: Considerable research effort has been focused on deciphering the immune response to SARS-CoV-2 infections and understanding the pathophysiology of COVID-19, including Long Covid syndrome. The hope is that knowledge gained from this research will be applied to studies of inflammatory processes in critical and chronic illnesses in the future.
Article
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Xiaoman Liu et al.
Summary: The spike protein of SARS-CoV-2 induces cell fusion, leading to an interferon response and nuclear damage. This response is mediated by the cGAS-STING pathway. The study uncovers the mechanism of the IFN response to SARS-CoV-2 infection.
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Lulu Han et al.
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Multidisciplinary Sciences
Shouheng Jin et al.
Summary: The study found that SARS-CoV-2 infection can modulate the SUMOylation of ACE2, a host receptor used for cell entry, leading to its stabilization and reduced degradation. By inhibiting ACE2 SUMOylation, it is possible to block SARS-CoV-2 infection.
NATURE COMMUNICATIONS
(2022)
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Wenbiao Wang et al.
Summary: This review article focuses on the signaling mechanisms of SARS-CoV-2 N protein in viral replication, cell death, and inflammation.
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
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Cell Biology
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Summary: SARS-CoV-2 infection impairs the disassembly of host stress granules (SGs) and promotes the aggregation of SG-related amyloid proteins, potentially increasing the risk of neurodegeneration.
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Biochemistry & Molecular Biology
Yi Zheng et al.
Summary: This study reveals the involvement of the stress response pathway and innate antiviral immunity in the pathogenic mechanism of SARS-CoV-2. NSP5 and N protein of SARS-CoV-2 were found to attenuate the formation of antiviral stress granules (avSG). NSP5 suppressed avSG formation and disrupted the RIG-I-MAVS complex to weaken the RIG-I-mediated antiviral response, while N protein specifically targeted cofactors upstream of RIG-I and affected the recognition of dsRNA by RIG-I.
SIGNAL TRANSDUCTION AND TARGETED THERAPY
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Marc Lipsitch et al.
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Microbiology
Ben Hu et al.
Summary: This review summarizes the research progress on SARS-CoV-2 and COVID-19, including virology characteristics, pathogenesis, and recent advances in treatment methods. Furthermore, it discusses in detail the potential wildlife hosts and zoonotic origin of this emerging virus.
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Summary: Pattern recognition receptors (PRRs) and inflammasomes play key roles in the anti-viral innate immune system by detecting viral molecular patterns and producing inflammatory cytokines to combat viral infections. Inflammasomes contribute to anti-viral responses by inducing cell death. Excessive innate immune responses may contribute to viral pathology.
BIOCHEMICAL PHARMACOLOGY
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Saleem Anwar et al.
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He Ren et al.
Summary: Research showed that SARS-CoV-2 infection could lead to the formation of micronuclei within cells, activating DNA damage response and cGAS-STING signaling, providing insights into the pathological effects of the infection and potential targets for COVID-19 therapy.
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Joel De la Cruz Enriquez et al.
Summary: SARS-CoV-2 infection induces oxidative stress and inflammation markers, inhibits mitochondrial function, and leads to cell death in leukocytes. This process is correlated with tissue damage and multi-organ failure, sustained by oxidative stress and inflammation.
FREE RADICAL RESEARCH
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Nemat Ali et al.
Summary: The study reveals that the SARS-CoV-2 N protein affects host cell stress granules formation, promoting viral replication and propagation, identified regulators of G3BP1/2 gene expression, and found imatinib and decitabine as potential drugs for COVID-19 treatment by modulating the expression of G3BP1/2 genes. Molecular docking analysis suggests that these drugs bind to G3BP1/2 with higher affinity than the SARS-CoV-2 N protein.
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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Multidisciplinary Sciences
Lingling Luo et al.
Summary: Understanding how SARS-CoV-2 disrupts stress granules (SGs) through interaction with the nucleocapsid (N) protein sheds light on the virus' ability to evade host antiviral defenses. This interaction plays a crucial role in viral production, highlighting the importance of studying these mechanisms in combatting COVID-19.
Review
Multidisciplinary Sciences
Juan Li et al.
Summary: Since the emergence of COVID-19 in Wuhan in 2019, the world has faced a devastating pandemic with millions of cases and fatalities. This article provides insights into the spread and genetic variations of the SARS-CoV-2 virus, emphasizes the importance of genomic surveillance, and highlights the international transmission of major variants identified late in 2020.
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Immunology
Hong Cai et al.
Summary: The study demonstrates the critical role of G3BP1 in immune responses induced by intracellular DNA and RNA, as its deletion leads to impaired cGAS activation and insufficient binding of RNA by RIG-I. Resveratrol suppresses type I IFN production by inhibiting G3BP1 and effectively alleviates intracellular nucleic acid-stimulated autoimmune responses in experimental mouse models for Aicardi-Goutières syndrome.
JOURNAL OF IMMUNOLOGY
(2021)
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Virology
Lulu Han et al.
Summary: The SARS-CoV-2 ORF9b protein inhibits the production of type I and type III interferons by targeting multiple molecules of innate antiviral signaling pathways, thus facilitating viral replication.
JOURNAL OF MEDICAL VIROLOGY
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Virology
Wei Liu et al.
Summary: The COVID-19 pandemic has posed a serious threat to global health, and research has found that activating the STING signaling pathway can effectively inhibit coronavirus infection, potentially serving as a promising target for future treatments against various strains of coronaviruses.
JOURNAL OF VIROLOGY
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Taisho Yamada et al.
Summary: Efficient immune responses against viral infection are determined by sufficient activation of nucleic acid sensor-mediated innate immunity. RIG-I plays a distinctive role as a restraining factor in the early phase of SARS-CoV-2 infection in human lung cells by recognizing the 3' untranslated region of the viral genome and inhibiting viral replication.
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Li-Qiu Wang et al.
Summary: The study reveals that the double-stranded DNA receptor AIM2 can sense the environmental pollutant perfluorooctane sulfonate, leading to inflammation and tissue damage through the activation of the AIM2 pathway.
NATURE COMMUNICATIONS
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Cell Biology
Dan Zhao et al.
Review
Immunology
Roberto Amadio et al.
Summary: The activation of cellular responses to DNA acts as a defense mechanism, but uncontrolled response can lead to autoimmune diseases. Dysregulated recognition of self-DNA is associated with type-I interferons and ISGs, while fine-tuned membrane trafficking and cytoskeletal dynamics play crucial roles.
FRONTIERS IN IMMUNOLOGY
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GuanQun Liu et al.
Summary: Conjugation of ISG15 plays a crucial role in activating the RIG-I-like receptor MDA5 and triggering antiviral responses, while SARS-CoV-2 suppresses MDA5 activation through direct de-ISGylation to evade innate immunity.
NATURE MICROBIOLOGY
(2021)
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Immunology
Fiachra Humphries et al.
Summary: This study describes a compound, diABZI-4, that activates stimulator of interferon genes (STING) and effectively limits SARS-CoV-2 replication in cells and animals. The administration of diABZI-4 intranasally in mice provided complete protection from severe respiratory disease caused by SARS-CoV-2. It induces a rapid, short-lived activation of STING, leading to transient proinflammatory cytokine production and lymphocyte activation in the lung, ultimately inhibiting viral replication. The study supports the use of diABZI-4 as a host-directed therapy for the treatment and prevention of COVID-19.
SCIENCE IMMUNOLOGY
(2021)
Article
Cell Biology
Shuai Wang et al.
Summary: Wang et al. found that the nucleocapsid protein of SARS-CoV-2 forms phase-separated condensates to repress antiviral immunity by inhibiting ubiquitination and aggregation of mitochondrial antiviral-signalling protein. They also identified a key acetylation site and mutations that impair the protein's phase separation with RNA, and developed a peptide disrupting this process to inhibit viral replication and enhance antiviral immunity.
NATURE CELL BIOLOGY
(2021)
Review
Genetics & Heredity
Kaiming Tao et al.
Summary: The emergence of multiple SARS-CoV-2 variants has significant impacts on the epidemiological and clinical aspects of the COVID-19 pandemic, including increased virus transmission rates, heightened risk of reinfection, and reduced effectiveness of neutralizing antibodies and vaccines. These variants have introduced new challenges to COVID-19 research, necessitating additional avenues of laboratory, epidemiological, and clinical studies.
NATURE REVIEWS GENETICS
(2021)
Review
Microbiology
Haitao Yang et al.
Summary: The COVID-19 pandemic caused by SARS-CoV-2 has led to an unprecedented global health crisis, with limited therapeutic options available. Understanding the structure and function of the 29 proteins encoded by SARS-CoV-2 is crucial for developing novel therapeutics and treatment interventions. These proteins play various roles in the viral life cycle, from entry into host cells to genome replication and transcription, highlighting their potential as targets for therapeutic interventions.
NATURE REVIEWS MICROBIOLOGY
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Bin Yang et al.
Summary: Persistent SARS-CoV-2 infection in COVID-19 patients is associated with immune suppression and reduced expression of ribosomal protein genes, as revealed by single-cell RNA sequencing and other data analysis.
NATURE COMMUNICATIONS
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Zhuo Zhou et al.
Summary: SARS-CoV-2 infection activates the host innate immune response through cytoplasmic DNA sensing pathway, involving cGAS and STING. Research shows that chromatin DNA can be transferred from the nucleus to the cytoplasm upon infection, triggering an immune alarm response. The study also highlights the essential roles of cGAS and STING in combating SARS-CoV-2, with potential therapeutic implications.
SIGNAL TRANSDUCTION AND TARGETED THERAPY
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Review
Toxicology
Vitor Pedro Targhetta et al.
Summary: In the context of the COVID-19 pandemic, the interaction of SARS-CoV-2 with host cells and its potential hijacking of mitochondria have brought attention to the impact on mitochondrial function and cell metabolism. The extrusion of mitochondrial DNA and subsequent proinflammatory responses play important roles in immune responses, with potential implications for therapeutic interventions. Further research on mtDNA receptors and signaling pathways could provide valuable insights into the immune processes and lung pathogenesis associated with SARS-CoV-2 infection.
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John S. Tregoning et al.
Summary: The development and rollout of vaccines have brought hope for controlling the COVID-19 pandemic, with vaccines proving highly effective in preventing disease. However, challenges remain in ensuring equitable access to vaccines globally, as well as lessons to be learned for controlling pandemics in the future.
NATURE REVIEWS IMMUNOLOGY
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Yaoxing Wu et al.
Summary: The study reveals that the nucleocapsid (N) protein of SARS-CoV-2 promotes the activation of the NF-κB signaling pathway, leading to inflammatory responses. Inhibiting liquid-liquid phase separation can weaken the regulatory function of this protein, offering a potential therapeutic target for severe pneumonia caused by COVID-19.
SIGNAL TRANSDUCTION AND TARGETED THERAPY
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Yajuan Rui et al.
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