The molecular mechanism of SARS-CoV-2 evading host antiviral innate immunity

Abstract

The newly identified Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has resulted in a global health emergency (COVID-19) because of its rapid spread and high mortality. Since the virus epidemic, many pathogenic mechanisms have been revealed, and virus-related vaccines have been successfully developed and applied in clinical practice. However, the pandemic is still developing, and new mutations are still emerging. Virus pathogenicity is closely related to the immune status of the host. As innate immunity is the body’s first defense against viruses, understanding the inhibitory effect of SARS-CoV-2 on innate immunity is of great significance for determining the target of antiviral intervention. This review summarizes the molecular mechanism by which SARS-CoV-2 escapes the host immune system, including suppressing innate immune production and blocking adaptive immune priming. Here, on the one hand, we devoted ourselves to summarizing the combined action of innate immune cells, cytokines, and chemokines to fine-tune the outcome of SARS-CoV-2 infection and the related immunopathogenesis. On the other hand, we focused on the effects of the SARS-CoV-2 on innate immunity, including enhancing viral adhesion, increasing the rate of virus invasion, inhibiting the transcription and translation of immune-related mRNA, increasing cellular mRNA degradation, and inhibiting protein transmembrane transport. This review on the underlying mechanism should provide theoretical support for developing future molecular targeted drugs against SARS-CoV-2. Nevertheless, SARS-CoV-2 is a completely new virus, and people’s understanding of it is in the process of rapid growth, and various new studies are also being carried out. Although we strive to make our review as inclusive as possible, there may still be incompleteness.

Non-structure protein ORF1ab (NSP8) in SARS-CoV-2 contains potential γδT cell epitopes

“…NSP8 initiates the synthesis of complementary short oligonucleotides and provides RNA primers required by NSP12 during viral replication and transcription (Imbert et al, 2006). It has been suggested that NSP8, being engaged in specific cytoplasmic foci, can form complexes with NSP7, NSP9, and NSP10 (Zhai et al, 2005;Achour, 2021) and suppress protein integration into cytoplasmic membrane thereby mitigate the interferon response of host cells (Banerjee et al, 2020;Gu et al, 2022). Recent studies highlighted the possibility of NSP8 as an antigenic target of SARS-CoV-2 (Ahmad et al, 2020;Ong et al, 2020).…”

Determination of soluble angiotensin-converting enzyme 2 in saliva samples and its association with nicotine

“…Moreover, our observed decrease of ACE2 levels due to ageing has been previously described and it was postulated as one of the causes for the increased mortality rate in elder patients ( Xie et al, 2006 ; Berni Canani et al, 2021 ). However, other authors have hypothesized that COVID-19 susceptibility in elderly can be related to the increase of ACE2 expression ( Narula et al, 2020 ; Gu et al, 2022 ).…”

Infectious Bronchitis Virus Nsp14 Degrades JAK1 to Inhibit the JAK-STAT Signaling Pathway in HD11 Cells

“…One is to block binding to ISRE and GAS by inhibiting STAT1 nuclear translocation. For the CoVs, SARS-CoV-2 and SARS-CoV ORF6 inhibit ISRE promoter activation by blocking STAT1 nuclear translocation but not phosphorylation [ 29 , 46 , 47 ]. However, in IBV-infected Vero cells, IBV-mediated inhibition of STAT1 nuclear translocation after IFN-β treatment is independent of accessory proteins [ 35 ].…”