Lysine 164 is critical for SARS-CoV-2 Nsp1 inhibition of host gene expression

Shen, Zhou; Zhang, Guangxu; Yang, Y.; Li, Mengxia; Yang, Siqi; Peng, Guiqing

doi:10.1099/jgv.0.001513

Cited by 26 publications

(26 citation statements)

References 55 publications

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“…Expression of SARS-CoV nsp1also inhibits cell proliferation and increases the number of cells in G0/G1 phase without affecting cell viability [64]. Likewise, SARS-CoV-2 nsp1 expression induces G0/G1 phase arrest [75]. Also, nsp1 of α-CoV, including TGEV, PRCV, SADS-CoV, PEDV, HCoV-229E, or HCoV-NL63, arrests the cell cycle at the G0/G1 phase in expressing cells [77].…”

Section: Cov Nsp1-induced Cell Cycle Arrestmentioning

confidence: 99%

Mechanisms of Coronavirus Nsp1-Mediated Control of Host and Viral Gene Expression

Nakagawa

Makino

2021

Cells

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Many viruses disrupt host gene expression by degrading host mRNAs and/or manipulating translation activities to create a cellular environment favorable for viral replication. Often, virus-induced suppression of host gene expression, including those involved in antiviral responses, contributes to viral pathogenicity. Accordingly, clarifying the mechanisms of virus-induced disruption of host gene expression is important for understanding virus–host cell interactions and virus pathogenesis. Three highly pathogenic human coronaviruses (CoVs), including severe acute respiratory syndrome (SARS)-CoV, Middle East respiratory syndrome (MERS)-CoV, and SARS-CoV-2, have emerged in the past two decades. All of them encode nonstructural protein 1 (nsp1) in their genomes. Nsp1 of SARS-CoV and MERS-CoV exhibit common biological functions for inducing endonucleolytic cleavage of host mRNAs and inhibition of host translation, while viral mRNAs evade the nsp1-induced mRNA cleavage. SARS-CoV nsp1 is a major pathogenic determinant for this virus, supporting the notion that a viral protein that suppresses host gene expression can be a virulence factor, and further suggesting the possibility that SARS-CoV-2 nsp1, which has high amino acid identity with SARS-CoV nsp1, may serve as a major virulence factor. This review summarizes the gene expression suppression functions of nsp1 of CoVs, with a primary focus on SARS-CoV nsp1 and MERS-CoV nsp1.

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Section: Cov Nsp1-induced Cell Cycle Arrestmentioning

confidence: 99%

Mechanisms of Coronavirus Nsp1-Mediated Control of Host and Viral Gene Expression

Nakagawa

Makino

2021

Cells

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“…On its hand, BRDT is required for expression of Ccna1 (Cyclin A1) during spermatogenesis [69,70]. Importantly, SARS-CoV-2 nsp1, which is involved in inhibition of host protein expression, has been shown to induce cell cycle arrest in G0/G1 phase [71].…”

Section: General Bet Functionsmentioning

confidence: 99%

Relevance of BET Family Proteins in SARS-CoV-2 Infection

Lara-Ureña

García-Domínguez

2021

Biomolecules

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The recent pandemic we are experiencing caused by the coronavirus disease 2019 (COVID-19) has put the world’s population on the rack, with more than 191 million cases and more than 4.1 million deaths confirmed to date. This disease is caused by a new type of coronavirus, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A massive proteomic analysis has revealed that one of the structural proteins of the virus, the E protein, interacts with BRD2 and BRD4 proteins of the Bromodomain and Extra Terminal domain (BET) family of proteins. BETs are essential to cell cycle progression, inflammation and immune response and have also been strongly associated with infection by different types of viruses. The fundamental role BET proteins play in transcription makes them appropriate targets for the propagation strategies of some viruses. Recognition of histone acetylation by BET bromodomains is essential for transcription control. The development of drugs mimicking acetyl groups, and thereby able to displace BET proteins from chromatin, has boosted interest on BETs as attractive targets for therapeutic intervention. The success of these drugs against a variety of diseases in cellular and animal models has been recently enlarged with promising results from SARS-CoV-2 infection studies.

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“…Noteworthily, the recent study demonstrated that the nsp1 protein of SARS-CoV-2 could bind to 40S and 80S ribosomes and interfered with cap-dependent translation in host cells (56). And the key residue in nsp1 to inhibit host gene expression, a lysine, has been proven to be located at amino acid site 164 (K164) (57).…”

Section: Interfere With Host Biological Activitiesmentioning

confidence: 99%

The Pathogenic Features of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): Possible Mechanisms for Immune Evasion?

Wang

Zhou

et al. 2021

Front. Immunol.

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Severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is a newly emerging, highly transmitted and pathogenic coronavirus that has caused global public health events and economic crises. As of March 4, 2021, more than 100 million people have been infected, more than 2 million deaths have been reported worldwide, and the numbers are continuing to rise. To date, a specific drug for this lethal virus has not been developed to date, and very little is currently known about the immune evasion mechanisms of SARS-CoV-2. The aim of this review was to summarize and sort dozens of published studies on PubMed to explore the pathogenic features of SARS-CoV-2, as well as the possible immune escape mechanisms of this virus.

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Lysine 164 is critical for SARS-CoV-2 Nsp1 inhibition of host gene expression

Cited by 26 publications

References 55 publications

Mechanisms of Coronavirus Nsp1-Mediated Control of Host and Viral Gene Expression

Mechanisms of Coronavirus Nsp1-Mediated Control of Host and Viral Gene Expression

Relevance of BET Family Proteins in SARS-CoV-2 Infection

The Pathogenic Features of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): Possible Mechanisms for Immune Evasion?

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