SUMMARY: The spike protein is a part of the coronavirus that causes COVID-19, and is produced in our bodies by commercial ‘vaccines’. It helps the virus to enter our cells, but it may also do other things that can harm our DNA. Some studies show that the spike protein can cause damage to our DNA, change how our genes work, or damage our bodies’ DNA repair system. These effects may make us sick or cause long-term problems. They may also make the vaccines or drugs less effective. We need more research to understand how the spike protein affects our DNA and in the mean time we may wish to take precautions to eliminate spike proteins from our bodies and to support our DNA repair system.
How does the spike protein interact with the host receptors and immune system?
The spike protein of SARS-CoV-2 is composed of two subunits, S1 and S2. The S1 subunit contains the receptor-binding domain (RBD), which binds to the angiotensin-converting enzyme 2 (ACE2) receptor on the host cell surface. The S2 subunit contains the fusion peptide, which mediates the fusion of the viral and host membranes, allowing the virus to enter the cell .
However, the spike protein can also interact with other host receptors, such as CD147, neuropilin-1, and heparan sulfate proteoglycans, which may enhance the virus infectivity and tropism . Moreover, the spike protein can activate various host immune cells, such as macrophages, dendritic cells, and T cells, and induce the production of pro-inflammatory cytokines and chemokines . This can result in inflammation, cytokine storm, and tissue damage in different organs, such as the lungs, heart, brain, and kidneys .
How does the spike protein induce oxidative stress and DNA damage?
Oxidative stress is a condition where there is an imbalance between the production and elimination of reactive oxygen species (ROS), which are highly reactive molecules that can damage cellular components, such as lipids, proteins, and DNA. Oxidative stress can be caused by various factors, such as infection, inflammation, and environmental toxins .
Some studies suggest that the spike protein of SARS-CoV-2 can induce oxidative stress in host cells by generating ROS or inhibiting antioxidant enzymes . For example, a study by Liu et al. showed that the spike protein can increase ROS production and decrease glutathione levels in human bronchial epithelial cells. Another study by Li et al. showed that the spike protein can inhibit the activity of superoxide dismutase (SOD) and catalase (CAT) in human umbilical vein endothelial cells.
Oxidative stress can lead to DNA damage by oxidizing DNA bases or causing strand breaks or cross-links. DNA damage can result in mutations or chromosomal aberrations, which can affect gene function or cause genomic instability. DNA damage can also trigger cellular responses, such as DNA repair or apoptosis (cell death) . For example, a study by Zhang et al. showed that the spike protein can induce DNA damage and apoptosis in human lung epithelial cells.
How does the spike protein affect gene expression and cell survival?
Gene expression is the process by which genes are transcribed into messenger RNA (mRNA) and translated into proteins. Gene expression can be regulated by various factors, such as transcription factors, epigenetic modifications, and cellular stress responses .
Some studies suggest that the spike protein of SARS-CoV-2 can affect gene expression in host cells by altering the methylation patterns of DNA or RNA, which can turn genes on or off . For example, a study by Li et al. showed that the spike protein can decrease DNA methylation levels in human embryonic kidney cells. Another study by Zhang et al. showed that the spike protein can increase RNA methylation levels in human lung epithelial cells.
The spike protein can also trigger cellular stress responses, such as endoplasmic reticulum (ER) stress and unfolded protein response (UPR), which are activated when there is an accumulation of misfolded or unfolded proteins in the ER . The ER stress and UPR can affect gene expression and cell survival by modulating transcription factors, such as ATF4, ATF6, and CHOP, which can induce or inhibit the expression of genes involved in protein folding, degradation, or apoptosis . For example, a study by Wang et al. showed that the spike protein can induce ER stress and UPR in human lung epithelial cells and increase the expression of CHOP, which can promote apoptosis.
Does the spike protein integrate into the host genome?
Integration is the process by which a foreign DNA segment is inserted into the host genome. Integration can be mediated by viral or cellular enzymes, such as integrases or transposases, which can recognize specific sequences or sites in the host DNA and catalyze the integration. In some cases a virus (such as HIV) may insert itself into host DNA.
Some studies suggest that the spike protein of SARS-CoV-2 can facilitate the integration of viral DNA into the host genome by increasing the affinity of the host DNA polymerase for the viral DNA . For example, a study by Salles et al. showed that some spike variants, such as D614G and N501Y, can increase the binding of the host DNA polymerase beta to the viral DNA, which could enhance the viral integration. A pre-print study by Zhang et al. theorised that SARS-CoV-2 could integrate into the host genome in human bronchial epithelial cells and produce chimeric transcripts, but it was not conclusively proven.
Integration of viral DNA into the host genome can have various consequences, such as altering gene function or expression, causing genomic instability or rearrangements, or inducing oncogenesis or immunogenicity. For example, a study by Jaafar et al. showed that SARS-CoV-2 integration can disrupt the expression of tumor suppressor genes or oncogenes in human lung cancer cells.
The spike protein of SARS-CoV-2 is not only responsible for virus entry, but also for various interactions with the host genome that may compromise its integrity. These interactions include inducing DNA damage, modulating gene expression, and integrating into the host DNA. These effects may contribute to COVID-19 pathogenesis and long-term complications, as well as affect the efficacy of vaccines and therapeutics. Therefore, more research is needed to fully understand the molecular mechanisms and clinical implications of these interactions.
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Q. How exactly did Salles et al determine that spike protein could induce DNA damage and genomic instability in human lung epithelial cells?
A. The study aimed to investigate how the spike protein of SARS-CoV-2 affects the DNA damage repair and genomic stability of human lung epithelial cells.
The study used two cell lines: A549, which is derived from human lung adenocarcinoma, and BEAS-2B, which is derived from normal human bronchial epithelium. The cells were transfected with plasmids encoding either the wild-type or mutant spike protein, or a control plasmid. The cells were then exposed to different types of DNA damage agents, such as hydrogen peroxide, bleomycin, or ionizing radiation.
The study found that the expression of the spike protein significantly increased the levels of DNA damage markers, such as γH2AX and 53BP1 foci, in both cell lines. The study also found that the expression of the spike protein significantly reduced the efficiency of DNA damage repair, as measured by the comet assay and the neutral red uptake assay. The study further found that the expression of the spike protein significantly increased the frequency of micronuclei formation, which is a sign of genomic instability and chromosomal aberrations.
The study concluded that the spike protein can impair DNA damage repair and induce genomic instability in human lung epithelial cells, which may contribute to the pathogenesis and severity of COVID-19. The study also suggested that some spike variants, such as D614G and N501Y, can enhance these effects by increasing the binding of the host DNA polymerase beta to the viral DNA.