Abstract
The coronavirus infectious disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains a world health concern and can cause severe disease and high mortality in susceptible groups. While vaccines offer a chance to treat disease, prophylactic and anti-viral treatments are still of vital importance, especially in context of the mutative ability of this group of viruses. Therefore, it is essential to elucidate the molecular mechanisms of viral entry, innate sensing and immune evasion of SARS-CoV-2, which control the triggers of the subsequent excessive inflammatory response. Viral evasion strategies directly target anti-viral immunity, counteracting host restriction factors and hijacking signalling pathways to interfere with interferon production. In Part I of this review, we examine SARS-CoV-2 viral entry and the described immune evasion mechanisms to provide a perspective on how the failure in initial viral sensing by infected cells can lead to immune dysregulation causing fatal COVID-19, discussed in Part II.
Highlights
Graphical AbstractBox 1: Why does your reviewed topic matter in the pandemic? The Coronavirus disease 2019 (COVID-19) pandemic is caused by a novel virus termed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
The coronavirus infectious disease 2019 (COVID-19) pandemic has had devastating global impacts on human health and the economy
In Part I of this review, we examine SARS-CoV-2 viral entry and the described immune evasion mechanisms to provide a perspective on how the failure in initial viral sensing by infected cells can lead to immune dysregulation causing fatal COVID-19, discussed in Part II
Summary
Box 1: Why does your reviewed topic matter in the pandemic? The Coronavirus disease 2019 (COVID-19) pandemic is caused by a novel virus termed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Viral sensing by the host cell is essential for the innate immune response to be triggered. It is pivotal to elucidate the mechanisms of viral entry, innate sensing and immune evasion of SARS-CoV-2, which can provide a basis for therapeutic development. SARS-CoV-2 encodes for proteins that counteract these viral recognition pathways or function as IFN antagonists, leading to reduced IFN signalling. Subsets of patients present with genetic mutations in the TLR3 and IRF7 signalling pathways, which lead to defective IFN responses and a worse outcome. This impaired sensing of virus may allow viral replication, which leads to cell damage and systematic immune dysregulation
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