Insights into pandemic respiratory viruses: manipulation of the antiviral interferon response by SARS-CoV-2 and influenza A virus

Liu, Guanqun; Gack, Michaela U.

doi:10.1016/j.coi.2022.102252

Cited by 9 publications

(8 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Suppression of IFN production is a major strategy of immune evasion utilised by SARS-CoV-2. Subjects with COVID-19 exhibit vastly delayed/reduced production of type-I/III IFNs compared with individuals infected with influenza virus [ 46 ]. Furthermore, in cells infected with SARS-CoV-2, expression of IFN-β and ISG56, a family of ISGs, peaks much later compared to cells infected with Sendai virus [ 47 ].…”

Section: Adaptation To Innate Interferon Signalling Can Results In Im...mentioning

confidence: 99%

On the Evolutionary Trajectory of SARS-CoV-2: Host Immunity as a Driver of Adaptation in RNA Viruses

Warger

Gaudieri

2022

Viruses

View full text Add to dashboard Cite

Host immunity can exert a complex array of selective pressures on a pathogen, which can drive highly mutable RNA viruses towards viral escape. The plasticity of a virus depends on its rate of mutation, as well as the balance of fitness cost and benefit of mutations, including viral adaptations to the host’s immune response. Since its emergence, SARS-CoV-2 has diversified into genetically distinct variants, which are characterised often by clusters of mutations that bolster its capacity to escape human innate and adaptive immunity. Such viral escape is well documented in the context of other pandemic RNA viruses such as the human immunodeficiency virus (HIV) and influenza virus. This review describes the selection pressures the host’s antiviral immunity exerts on SARS-CoV-2 and other RNA viruses, resulting in divergence of viral strains into more adapted forms. As RNA viruses obscure themselves from host immunity, they uncover weak points in their own armoury that can inform more comprehensive, long-lasting, and potentially cross-protective vaccine coverage.

show abstract

Section: Adaptation To Innate Interferon Signalling Can Results In Im...mentioning

confidence: 99%

On the Evolutionary Trajectory of SARS-CoV-2: Host Immunity as a Driver of Adaptation in RNA Viruses

Warger

Gaudieri

2022

Viruses

View full text Add to dashboard Cite

show abstract

“…cGAS–STING–NLRP3 pathway ameliorates the pathology in inflammatory conditions linked with cytosolic DNA sensing [ 112 ]. However, the pathway exacerbated COVID-19 by sensing cytosolic DNA from senescent cells or aberrant DNA by SARS-CoV-2 [ 113 ]. We have experiences based on clinical practice prescribing aspirin, dapsone, and dexamethasone to inhibit cGAS-STING activation by SARS-CoV-2 [ 6 ].…”

Section: Treatment Mechanism Of Triadmentioning

confidence: 99%

Treatment mechanism of immune triad from the repurposing drug against COVID-19

Lee

2023

Translational Medicine of Aging

View full text Add to dashboard Cite

“…In uenza A virus (IAV) and SARS-CoV dysregulate human innate immune responses. Severe in uenza exhibits distinct cytokine patterns similar to SARS-CoV-2's ability to suppress immune responses 19 . We analyzed diverse relationships with immune-mediated VRDs, pneumonia, COPD, and AD through national health electronic data interchange (EDI) systems.…”

Section: Study Strategymentioning

confidence: 99%

The study of whether acquired Mendelian diseases are the origin of Alzheimer’s disease from viral respiratory diseases.

Lee

2023

Preprint

View full text Add to dashboard Cite

We must study viral RNA infection, sustained interferon response, acetylcholine excess, and developing Alzheimer’s disease (AD). We analyzed viral respiratory disease (VRD) (+)/(−) and dapsone (DDS) (+)/(−) groups. ANOVA calculator, logistic regression analysis, and Mann-Whitney U Test Calculator were used to examine the association of VRDs, COPD, and anti-AD drugs (AADs) with AD. A total of 107 subjects from 2005 to 2021 developed COPD. The DDS (+) AAD (-) and DDS (-) AAD (+) groups were strongly positively correlated with all COPD subjects. COPD develops into AD without dapsone, and AAD exacerbates AD through COPD. Ten AD among ninety-three non-COPD patients occurred in 2010 since the endemic. Viral infections set a direct pathway into AD directly without COPD. The endemic causes bronchitis, COPD, and AD. Acquired Mendelian up-regulation might set a direct pathway into AD as an origin.

show abstract

Insights into pandemic respiratory viruses: manipulation of the antiviral interferon response by SARS-CoV-2 and influenza A virus

Cited by 9 publications

References 52 publications

On the Evolutionary Trajectory of SARS-CoV-2: Host Immunity as a Driver of Adaptation in RNA Viruses

On the Evolutionary Trajectory of SARS-CoV-2: Host Immunity as a Driver of Adaptation in RNA Viruses

Treatment mechanism of immune triad from the repurposing drug against COVID-19

The study of whether acquired Mendelian diseases are the origin of Alzheimer’s disease from viral respiratory diseases.

Contact Info

Product

Resources

About