Effect of ORF7 of SARS-CoV-2 on the Chemotaxis of Monocytes and Neutrophils In Vitro.
Gang WangJun GuanGuojun LiFengtian WuQin YangChunhong HuangJunwei ShaoLichen XuZixuan GuoQihui ZhouHaihong ZhuZhi ChenPublished in: Disease markers (2021)
Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently the most significant public health threat worldwide. Patients with severe COVID-19 usually have pneumonia concomitant with local inflammation and sometimes a cytokine storm. Specific components of the SARS-CoV-2 virus trigger lung inflammation, and recruitment of immune cells to the lungs exacerbates this process, although much remains unknown about the pathogenesis of COVID-19. Our study of lung type II pneumocyte cells (A549) demonstrated that ORF7, an open reading frame (ORF) in the genome of SARS-CoV-2, induced the production of CCL2, a chemokine that promotes the chemotaxis of monocytes, and decreased the expression of IL-8, a chemokine that recruits neutrophils. A549 cells also had an increased level of IL-6. The results of our chemotaxis Transwell assay suggested that ORF7 augmented monocyte infiltration and reduced the number of neutrophils. We conclude that the ORF7 of SARS-CoV-2 may have specific effects on the immunological changes in tissues after infection. These results suggest that the functions of other ORFs of SARS-CoV-2 should also be comprehensively examined.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- coronavirus disease
- public health
- induced apoptosis
- dendritic cells
- cell cycle arrest
- poor prognosis
- high throughput
- cell death
- gene expression
- signaling pathway
- intensive care unit
- dna methylation
- early onset
- cell proliferation
- single cell
- pi k akt
- high glucose
- stress induced
- diabetic rats
- mechanical ventilation
- community acquired pneumonia