SARS-CoV-2 ORF6 protein targets TRIM25 for proteasomal degradation to diminish K63-linked RIG-I ubiquitination and type-I interferon induction

Article Multidisciplinary Sciences

The coding capacity of SARS-CoV-2

Yaara Finkel et al.

Summary: A high-resolution map of coding regions in the SARS-CoV-2 genome enables the identification of 23 unannotated open reading frames and quantification of the expression of canonical viral open reading frames.

NATURE (2021)

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Article Cell Biology

MDA5 Governs the Innate Immune Response to SARS-CoV-2 in Lung Epithelial Cells

Xin Yin et al.

Summary: Recent studies show that cellular responses to SARS-CoV-2 infection may influence disease severity, with MDA5 and LGP2 primarily regulating IFN induction in lung epithelial cells. Further analysis revealed that viral intermediates specifically activate the IFN response through MDA5-mediated sensing, and transcription factors IRF3, IRF5, and NF-kappa B/p65 play key roles in regulating the IFN response during SARS-CoV-2 infection. These findings provide valuable insights into the molecular mechanisms of innate immune recognition and signaling response to SARS-CoV-2.

CELL REPORTS (2021)

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Article Immunology

SARS-CoV-2 proteases PLpro and 3CLpro cleave IRF3 and critical modulators of inflammatory pathways (NLRP12 and TAB1): implications for disease presentation across species

Mehdi Moustaqil et al.

Summary: The study revealed that the proteases NSP3 and NSP5 of SARS-CoV-2 can cleave proteins involved in host immune responses, shedding light on the mechanisms behind enhanced inflammatory responses in COVID-19 patients. The direct cleavage of specific proteins by these proteases provides insights into the pathophysiology of the disease.

EMERGING MICROBES & INFECTIONS (2021)

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Article Immunology

Characterization of SARS-CoV-2 ORF6 deletion variants detected in a nosocomial cluster during routine genomic surveillance, Lyon, France

Gregory Queromes et al.

Summary: A study on SARS-CoV-2 revealed a nosocomial transmission of an ORF6 deletion variant, potentially involving fecal transmission, triggering specific host immune responses. These variants did not affect the severity of the disease in patients, but induced differences in host immune responses.

EMERGING MICROBES & INFECTIONS (2021)

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Correction Microbiology

SARS-CoV-2 suppresses IFNβ production mediated by NSP1, 5, 6, 15, ORF6 and ORF7b but does not suppress the effects of added interferon (vol 17, e1009800, 2021)

Maya Shemesh et al.

PLOS PATHOGENS (2021)

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Article Immunology

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Membrane (M) and Spike (S) Proteins Antagonize Host Type I Interferon Response

Qi Zhang et al.

Summary: The study identified that SARS-CoV-2 membrane protein and spike protein antagonize the IFN-I antiviral response through different mechanisms, inhibiting the nuclear translocation of IRF3 and blocking the interaction between STAT1 and JAK1. This research enhances our understanding of SARS-CoV-2 pathogenesis and suggests new therapeutic targets for the treatment of COVID-19.

FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY (2021)

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Review Microbiology

Innate Immunity Evasion Strategies of Highly Pathogenic Coronaviruses: SARS-CoV, MERS-CoV, and SARS-CoV-2

Jin-Yan Li et al.

Summary: The article reviews recent studies on the interference and infection process of highly pathogenic human coronaviruses (HP-hCoVs) in cells. HP-hCoVs employ various strategies to suppress immune responses, which is important for understanding the viral pathogenesis and developing antiviral therapies.

FRONTIERS IN MICROBIOLOGY (2021)

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Article Multidisciplinary Sciences

Multilevel proteomics reveals host perturbations by SARS-CoV-2 and SARS-CoV

Alexey Stukalov et al.

Summary: The study reports a concurrent multi-omics analysis of SARS-CoV-2 and SARS-CoV, revealing both distinct and common molecular mechanisms between these closely related coronaviruses, as well as their impact on the host cell proteome. The results of this study may provide insights into the design of virus- and host-directed therapies for these coronaviruses.

NATURE (2021)

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Article Microbiology

SARS-CoV-2 ORF6 Disrupts Bidirectional Nucleocytoplasmic Transport through Interactions with Rae1 and Nup98

Amin Addetia et al.

Summary: SARS-CoV-2 infection results in the accumulation of nuclear mRNA, attributed to the accessory protein ORF6 which interacts with Rae1 and Nup98 to trap host mRNA in the nucleus. Both SARS-CoV and SARS-CoV-2 ORF6 block the nuclear import of host proteins through interactions with Rae1 and Nup98, potentially preventing host cells from responding to viral infection.

MBIO (2021)

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Article Cell Biology

Systematic functional analysis of SARS-CoV-2 proteins uncovers viral innate immune antagonists and remaining vulnerabilities

Manuel Hayn et al.

Summary: SARS-CoV-2 proteins synergize to counteract innate immune responses, but they are vulnerable to type II and III interferons. Experimental results show potent inhibition of SARS-CoV-2 infection by interferon-gamma and lambda 1, highlighting potential for effective antiviral approaches.

CELL REPORTS (2021)

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Article Microbiology

ISG15-dependent activation of the sensor MDA5 is antagonized by the SARS-CoV-2 papain-like protease to evade host innate immunity

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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Article Biochemistry & Molecular Biology

SARS-CoV-2 sensing by RIG-I and MDA5 links epithelial infection to macrophage inflammation

Lucy G. Thorne et al.

Summary: SARS-CoV-2 infection leads to broad-spectrum immunopathological diseases, exacerbated by inflammatory co-morbidities. Research shows that the virus replicates rapidly in lung epithelial cells and triggers a robust innate immune response, affecting macrophage activation through inflammatory mediators produced during infection. Further exacerbation of the local inflammatory environment occurs when macrophages or epithelial cells are primed with exogenous inflammatory stimuli.

EMBO JOURNAL (2021)

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Article Multidisciplinary Sciences

SARS-CoV-2 viral proteins NSP1 and NSP13 inhibit interferon activation through distinct mechanisms

Christine Vazquez et al.

Summary: The SARS-CoV-2 virus blocks interferon signaling and reduces activation of NF-kappa B through distinct mechanisms, bypassing multiple innate immune activation pathways.

PLOS ONE (2021)

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Article Multidisciplinary Sciences

Translational shutdown and evasion of the innate immune response by SARS-CoV-2 NSP14 protein

Jack Chun-Chieh Hsu et al.

Summary: SARS-CoV-2 shuts down host innate immune responses through the translation inhibition activity of NSP14, revealing insights into the pathogenesis of the virus.

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2021)

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Article Immunology

RIG-I-Like Receptor-Mediated Recognition of Viral Genomic RNA of Severe Acute Respiratory Syndrome Coronavirus-2 and Viral Escape From the Host Innate Immune Responses

Takahisa Kouwaki et al.

Summary: RIG-I-like receptors (RLR), including RIG-I and MDA5, are crucial for the innate immune response to SARS-CoV-2, with both proteins involved in regulating cytokine expression. Transfection of viral RNA regions and viral proteins have effects on the immune response generation.

FRONTIERS IN IMMUNOLOGY (2021)

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Article Biochemistry & Molecular Biology

A dual-role of SARS-CoV-2 nucleocapsid protein in regulating innate immune response

Yinghua Zhao et al.

Summary: The N protein of SARS-CoV-2 has a dual regulatory effect on innate immune responses, inhibiting signaling at low doses and promoting inflammation at high doses. This mechanism could help understand the pathogenesis of SARS-CoV-2 and develop better strategies for controlling COVID-19.

SIGNAL TRANSDUCTION AND TARGETED THERAPY (2021)

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Review Biochemistry & Molecular Biology

Immune evasion of SARS-CoV-2 from interferon antiviral system

Yuan-Qin Min et al.

Summary: The ongoing COVID-19 pandemic caused by SARS-CoV-2 has led to unprecedented medical and socioeconomic crises, with viral proteins showing potential antagonistic effects against IFN responses. Understanding the strategies used by SARS-CoV-2 to evade innate immunity, particularly the antiviral IFN responses, will not only help elucidate the infection and pathogenesis, but also aid in the development of antiviral intervention therapies.

COMPUTATIONAL AND STRUCTURAL BIOTECHNOLOGY JOURNAL (2021)

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Letter Biochemistry & Molecular Biology

SARS-CoV-2 non-structural protein 13 (nsp13) hijacks host deubiquitinase USP13 and counteracts host antiviral immune response

Guijie Guo et al.

SIGNAL TRANSDUCTION AND TARGETED THERAPY (2021)

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Review Microbiology

Coronavirus biology and replication: implications for SARS-CoV-2

Philip V'kovski et al.

Summary: This review discusses key aspects of coronavirus biology and their implications for SARS-CoV-2 infections, treatment, and prevention strategies. Understanding virus-host interactions at the molecular level is crucial for developing effective intervention strategies. Summarizing the discoveries of SARS-CoV-2 infection and comparing it with other coronaviruses will support future preparedness and combat strategies.

NATURE REVIEWS MICROBIOLOGY (2021)

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Article Immunology

SARS-CoV-2 membrane glycoprotein M antagonizes the MAVS-mediated innate antiviral response

Yu-Zhi Fu et al.

Summary: A novel SARS-related coronavirus (SARS-CoV-2) has emerged as a serious pathogen causing high morbidity and mortality. The membrane glycoprotein M of SARS-CoV-2 was identified as a negative regulator of the innate immune response by impairing MAVS aggregation and downstream signaling, thus evading the innate antiviral response.

CELLULAR & MOLECULAR IMMUNOLOGY (2021)

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Editorial Material Microbiology