Devil's tools: SARS-CoV-2 antagonists against innate immunity

Xu, Duo; Biswal, Mahamaya; Neal, Arrmund; Hai, Rong

doi:10.1016/j.crviro.2021.100013

Cited by 19 publications

(27 citation statements)

References 82 publications

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“…Consistent with these studies, a dysregulation of the IFN-I signaling was observed here which was characterized by a reduction in several ISGs expression (Figure 5); however only ORF7a seemed to be a potent antagonist of IFN-I. What seems clear is that SARS-CoV-2 has evolved ways of using accessory proteins to subvert the IFN response (Martin-Sancho et al, 2021;Xu et al, 2021), although the antagonistic mechanism requires further study.…”

Section: Discussionsupporting

confidence: 84%

Antiviral immune responses, cellular metabolism and adhesion are differentially modulated by SARS-CoV-2 ORF7a or ORF7b

García-García

Fernandez-Rodriguez

Redondo

et al. 2022

Preprint

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SARS-CoV-2, the causative agent of the present COVID-19 pandemic, possesses eleven accessory proteins encoded in its genome, and some have been implicated in facilitating infection and pathogenesis through their interaction with cellular components. Among these proteins, accessory protein ORF7a and ORF7b functions are poorly understood. In this study, A549 cells were transduced to express ORF7a and ORF7b, respectively, to explore more in depth the role of each accessory protein in the pathological manifestation leading to COVID-19. Bioinformatic analysis and integration of transcriptome results identified defined canonical pathways and functional groupings revealing that after expression of ORF7a or ORF7b, the lung cells are potentially altered to create conditions more favorable for SARS-CoV-2, by inhibiting the IFN-I response, increasing proinflammatory cytokines release, and altering cell metabolic activity and adhesion. Based on these results, it is reasonable to suggest that ORF7a and ORF7b could be targeted by new therapies or used as future biomarkers during this pandemic.

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Section: Discussionsupporting

confidence: 84%

Antiviral immune responses, cellular metabolism and adhesion are differentially modulated by SARS-CoV-2 ORF7a or ORF7b

García-García

Fernandez-Rodriguez

Redondo

et al. 2022

Preprint

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“…14 Notably, SARS-CoV-2 proteins known to inhibit the host cell interferon response including S, NSP3, NSP6, NSP14, nucleocapsid (N), and membrane (M) are mutated in the Omicron variant. 15 Antiviral testing indicated a similar sensitivity of Omicron and Delta isolates to EIDD-1931, PF-07321332, remdesivir, favipravir, ribavirin, nafamostat, camostat, and aprotinin and, hence, to a range of drugs representing different mechanisms of action (Fig. 1e).…”

mentioning

confidence: 87%

Reduced interferon antagonism but similar drug sensitivity in Omicron variant compared to Delta variant of SARS-CoV-2 isolates

et al. 2022

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“…Taken together, these data show that Omicron viruses are less effective than Delta viruses in antagonising the interferon response in human cells, which may contribute to the lower pathogenicity of the Omicron variant observed in patients [21,22]. Notably, SARS-CoV-2 proteins known to inhibit the host cell interferon response including S, NSP3, NSP6, NSP14, nucleocapsid (N), and membrane (M) are mutated in the Omicron variant [23,24].…”

Section: Figurementioning

confidence: 99%

Reduced interferon antagonism but similar drug sensitivity in Omicron variant compared to Delta variant SARS-CoV-2 isolates

Bojkova

Widera

Ciesek

et al. 2022

Preprint

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The SARS-CoV-2 Omicron variant is currently causing a large number of infections in many countries. A number of antiviral agents are approved or in clinical testing for the treatment of COVID-19. Despite the high number of mutations in the Omicron variant, we here show that Omicron isolates display similar sensitivity to eight of the most important anti-SARS-CoV-2 drugs and drug candidates (including remdesivir, molnupiravir, and PF-07321332, the active compound in paxlovid), which is of timely relevance for the treatment of the increasing number of Omicron patients. Most importantly, we also found that the Omicron variant displays a reduced capability of antagonising the host cell interferon response. This provides a potential mechanistic explanation for the clinically observed reduced pathogenicity of Omicron variant viruses compared to Delta variant viruses.

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Devil's tools: SARS-CoV-2 antagonists against innate immunity

Cited by 19 publications

References 82 publications

Antiviral immune responses, cellular metabolism and adhesion are differentially modulated by SARS-CoV-2 ORF7a or ORF7b

Antiviral immune responses, cellular metabolism and adhesion are differentially modulated by SARS-CoV-2 ORF7a or ORF7b

Reduced interferon antagonism but similar drug sensitivity in Omicron variant compared to Delta variant of SARS-CoV-2 isolates

Reduced interferon antagonism but similar drug sensitivity in Omicron variant compared to Delta variant SARS-CoV-2 isolates

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