Spike protein dna damage full#

The reliability of the results and conclusions presented have therefore been undermined. Both the chosen construct of the spike plasmid that contained a C-terminal fused with 6xHis tag and use of a GFP reporter system under overexpression conditions in the protocol were identified as having the potential to introduce significant ambiguity regarding the nature of the reported observations. I am BAFFLED (or am I, 😉) as to why this paper was retracted.Īdhering to our complaint procedure, an investigation was conducted.

Spike protein dna damage full#

Just because the full length Spike vaccine WAS NOT STUDIED DOES NOT INVALIDATE THE FINDINGS. EVEN IF the contested conclusions about the Spike’s ability to impair adaptive immunity, the DNA damage repair impairment, I believe, was soundly shown. However, what I DO NOT understand is why another paper showing how the Spike impairs DNA damage repair and impairs adaptive immunity. Micronucleus production, activation of DNA damage response and cGAS-STING signaling in syncytia induced by SARS-CoV-2 infection Since activation of these signaling pathways were known to be associated with cellular catastrophe and aberrant immune activation, these findings help explain the pathological effects of SARS-CoV-2 infection at cellular and molecular levels, and provide novel potential targets for COVID-19 therapy. Remarkably, these micronuclei were manifested with a high level of activation of both DNA damage response and cGAS-STING signaling, as indicated by micronucleus translocation of γH2Ax and cGAS, and upregulation of their respective downstream target genes. Here, we reported that viral infection could induce syncytia formation within cells expressing ACE2 and the SARS-CoV-2 spike protein, leading to the production of micronuclei with an average rate of about 4 per syncytium (> 93%). The above figure is from a paper which found that the Spike Protein is indeed inducing a high level of DNA damage response. h Expression of NOXA, GADD45A, SLC7A11, PAI1 and MYC were analyzed by quantitative RT-PCR 24 h post spike transfection in Hela-ACE2 cells. Data are mean ± SD of triple quantification. All results were normalized by the expression of β-actin. e–g Expression of γH2AX and p53 proteins in Hela-ACE2 cells 24 h post transfection by Western blot (e) and quantification (f, g). c and d Quantification of micronuclei γH2Ax foci in Hela-ACE2 cells transfected by spike protein (c) or infected by SARS-CoV-2 (d). Scale bars: 50 μm for the left image, 20 μm for zoomed images in the middle and 1 μm for multi-channel images on the right. Zoomed images on the right indicate colocalization between γH2Ax and micronuclei in syncytia. Cells were stained with antibodies against γH2Ax protein in green. a and b Immunofluorescent images of Hela-ACE2 cells expressing exogenous SARS-CoV-2 spike glycoprotein (a) or infected by SARS-CoV-2 (b). Activation of DNA damage pathway in syncytia induced by SARS-CoV-2 infection and Spike-ACE2 expression.