By Daniel Brouse
SARS-CoV-2 and the results of COVID-19 cause long-term immune system dysfunction. That is to say COVID results in a compromised immune system.
* SARS-CoV-2 infection weakens immune-cell response
The magnitude and quality of a key immune cell’s response to vaccination with two doses of the Pfizer-BioNTech COVID-19 vaccine were considerably lower in people with prior SARS-CoV-2 infection compared to people without prior infection, a study has found. In addition, the level of this key immune cell that targets the SARS-CoV-2 spike protein was substantially lower in unvaccinated people with COVID-19 than in vaccinated people who had never been infected. Importantly, people who recover from SARS-CoV-2 infection and then get vaccinated are more protected than people who are unvaccinated. These findings suggest that the virus damages an important immune-cell response.
* Destruction of Good Gut Bacteria Resulting in a Compromised Immune System
Gut microbiome composition was significantly altered in patients with COVID-19 compared with non-COVID-19 individuals.
* Dysfunctional Kynurenine Pathway
“Targeted and untargeted metabolomics analyses identified altered tryptophan metabolism into the kynurenine pathway, which regulates inflammation and immunity.”
* Down Regulating NAD+
“NAD regulates the inflammatory response in immune and non-immune cells through Sirtuins. Epigenetic regulation of histones and non-histone proteins is induced by sirtuins and is essential for the development, reprogramming, and differentiation of the immune system and its related pathologies. A deregulation of the NAD+ levels has been associated with metabolic diseases and aging-related diseases, including neurodegeneration, defective immune responses, and cancer.”
* Up Regulating IDO
Indoleamine 2,3-dioxygenase (IDO) is an immune checkpoint molecule in the sense that it is an immunomodulatory enzyme produced by alternatively activated macrophages and other immunoregulatory cells. IDO is known to suppress T and NK cells, generate Tregs and myeloid-derived suppressor cells, and also supports angiogenesis.
* Rogue Antibodies
Autoantibodies are antibodies (immune proteins) that mistakenly attack a person’s own healthy tissues and organs. SARS-CoV-2 infection, is associated with many different clinical features that are commonly found in autoimmune diseases, including arthralgias, myalgias, fatigue, sicca, and rashes.
* Dysregulation of the innate immune system, i.e. “cytokine storm”
It is important to note that the severity of disease in humans is not determined only by virus replication but also by the host immune response to the infection, which may lead to dysregulation of the innate immune system, i.e. “cytokine storm” (Omicron SARS-CoV-2 can infect faster and better)
* Reinfection Greater Risks & Exacerbates Underlying Conditions
The evidence shows that reinfection further increases risks of death, hospitalization and damage to multiple organ systems. COVID exacerbates underlying conditions including pulmonary, cardiovascular, hematological, diabetes, gastrointestinal, kidney, mental heal<th, musculoskeletal and neurological disorders
* Post–COVID-19 Associated with Immune Cell Infiltration and Altered Gene Expression
COVID causes long-term immune dysfunction. “These findings indicate that T cell–mediated inflammation persists in the olfactory epithelium long after SARS-CoV-2 has been eliminated from the tissue, suggesting a mechanism for long-term post–COVID-19 smell loss.”
* Elevated Cytokines and Low Iron
Defects in iron homeostasis, dysregulated erythropoiesis contribute to inefficient oxygen transport, inflammatory imbalances, and persistent symptoms. The information on autoimmune diseases emphasizes that an excessive release of cytokines, which are signaling molecules involved in immune responses, can lead to an exaggerated inflammatory response. This heightened inflammation has the potential to damage tissues and contribute to autoimmune diseases, where the immune system mistakenly attacks healthy cells.
Also see: COVID-19: Increased Risk of Autoimmune Diseases