The battle between host and SARS-CoV-2: Innate immunity and viral evasion strategies

Zhang, Shilei; Wang, Lulan; Cheng, Genhong

doi:10.1016/j.ymthe.2022.02.014

Cited by 57 publications

(45 citation statements)

References 177 publications

(190 reference statements)

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“…At the cell surface, S protein can result in the fusion of an infected cell with adjacent, uninfected cells, leading to the formation of large, multinucleate syncytia. This enables the spread of infection independent of the action of extracellular virus, thereby providing some measure of escape from immune surveillance [ 18 , 24 ].…”

Section: Rna Virusesmentioning

confidence: 99%

Potential Resistance of SARS-CoV-2 Main Protease (Mpro) against Protease Inhibitors: Lessons Learned from HIV-1 Protease

Mótyán

Mahdi

Hoffka

et al. 2022

IJMS

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Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome 2 (SARS-CoV-2), has been one of the most devastating pandemics of recent times. The lack of potent novel antivirals had led to global health crises; however, emergence and approval of potent inhibitors of the viral main protease (Mpro), such as Pfizer’s newly approved nirmatrelvir, offers hope not only in the therapeutic front but also in the context of prophylaxis against the infection. By their nature, RNA viruses including human immunodeficiency virus (HIV) have inherently high mutation rates, and lessons learnt from previous and currently ongoing pandemics have taught us that these viruses can easily escape selection pressure through mutation of vital target amino acid residues in monotherapeutic settings. In this paper, we review nirmatrelvir and its binding to SARS-CoV-2 Mpro and draw a comparison to inhibitors of HIV protease that were rendered obsolete by emergence of resistance mutations, emphasizing potential pitfalls in the design of inhibitors that may be of important relevance to the long-term use of novel inhibitors against SARS-CoV-2.

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Section: Rna Virusesmentioning

confidence: 99%

Potential Resistance of SARS-CoV-2 Main Protease (Mpro) against Protease Inhibitors: Lessons Learned from HIV-1 Protease

Mótyán

Mahdi

Hoffka

et al. 2022

IJMS

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“…An increasing body of evidence indicates that SARS-CoV-2 enters the epithelial cells of the respiratory tract and lungs and epithelial and nonepithelial cells of other organs that express the ACE2 receptor, which triggers an antiviral immune response upon detection of the virus ( Sungnak et al, 2020 ; Zhang et al, 2022 ). SARS-CoV-2 infects the type II pneumocytes by binding its S protein with the angiotensin-converting enzyme 2 (ACE2) receptor exposed on the surface of the pneumocyte membrane.…”

Section: Supporting Evidencementioning

confidence: 99%

Exploiting Extracellular Vesicles Strategies to Modulate Cell Death and Inflammation in COVID-19

et al. 2022

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The coronavirus disease (COVID-19) is responsible for more than 5 million deaths worldwide, with respiratory failure being the most common clinical presentation. COVID-19 complications still present a considerable burden on healthcare systems, and signs of the post-COVID syndrome are concerns for potential long-term damages. An increasing body of evidence highlights extracellular vesicles’ (EVs) relevance in modulating inflammation and cell death in the diseases related to these processes. Several types of EVs-based investigational new drugs against COVID-19 have been approved by the US Food and Drug Administration to initiate a Phase I/II trial under an Investigational New Drug protocol. EVs can be employed as natural drug delivery nanoparticle-based systems due to their inherent potential in transferring material between cells, their natural origin, and their capability to encapsulate various biological molecules, offering an exciting alternative for administering drugs acting on the cell cycle control. In this context, small-molecule inhibitors of Mouse Double Minute 2 (MDM2) such as Nutlin-3 and Idasanutlin by promoting p53 survival and its antiviral activity might be helpful to modulate the IFN signalling pathway and reduce the overall pro-inflammatory burden.

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“…In response, SARS-CoV-2 has adapted secondary functions for many of its proteins ( Table 1 ) in order to subvert the host immune response ( Figure 4 ). These include evading PRR recognition, blocking PRR-mediated signaling cascades, the modulation of ubiquitination and deubiquitination, viral protease-mediated cleavage, and shutting down host translation [ 80 ].…”

Section: The Role Of Sars-cov-2 Proteins In Disrupting Innate Immune ...mentioning

confidence: 99%

“…For example, nsp5 targets the host immune response by interfering with RIG-I ubiquitination and also disrupts the formation of antiviral stress granules (avSG) [ 101 , 102 ]. It also cleaves RFN20, which is an antiviral ISG, as well as NLRP12 and TAB1, which are two important regulators of inflammation, contributing to abnormal cytokine expression and general immune dysregulation [ 80 , 103 ].…”

Section: The Role Of Sars-cov-2 Proteins In Disrupting Innate Immune ...mentioning

confidence: 99%

The Evolutionary Dance between Innate Host Antiviral Pathways and SARS-CoV-2

Aliyari

Quanquin

Pernet³

et al. 2022

Pathogens

Self Cite

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Compared to what we knew at the start of the SARS-CoV-2 global pandemic, our understanding of the interplay between the interferon signaling pathway and SARS-CoV-2 infection has dramatically increased. Innate antiviral strategies range from the direct inhibition of viral components to reprograming the host’s own metabolic pathways to block viral infection. SARS-CoV-2 has also evolved to exploit diverse tactics to overcome immune barriers and successfully infect host cells. Herein, we review the current knowledge of the innate immune signaling pathways triggered by SARS-CoV-2 with a focus on the type I interferon response, as well as the mechanisms by which SARS-CoV-2 impairs those defenses.

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The battle between host and SARS-CoV-2: Innate immunity and viral evasion strategies

Cited by 57 publications

References 177 publications

Potential Resistance of SARS-CoV-2 Main Protease (Mpro) against Protease Inhibitors: Lessons Learned from HIV-1 Protease

Potential Resistance of SARS-CoV-2 Main Protease (Mpro) against Protease Inhibitors: Lessons Learned from HIV-1 Protease

Exploiting Extracellular Vesicles Strategies to Modulate Cell Death and Inflammation in COVID-19

The Evolutionary Dance between Innate Host Antiviral Pathways and SARS-CoV-2

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