COVID-19 can cause a severe immune response known as a cytokine storm, leading to poor prognosis and potentially fatal outcomes.
The virus triggers excessive infiltration of immune cells, such as macrophages and T-helper 17 cells.
“SARS-CoV-2 can trigger an overactive immune response, leading to the release of large amounts of pro-inflammatory cytokines.
This excessive cytokine release can cause widespread inflammation, leading to damage in various organs, including the lungs, heart, and kidneys.”
COVID-19 rapidly increases senescent and exhausted T cells, particularly CD4 and CD8 T cells.
Both mild and severe COVID-19 cases showed increased markers of T-cell exhaustion and senescence with more pronounced changes in severe cases.
“In the blood of the long COVID patients, the team [at the University of Alberta] found higher levels of various proteins related to systemic inflammation—especially galectin-9 and artemin.. higher levels of galectin-9 in patients are associated with increased inflammation and brain fog.. higher levels of artemin are associated with widespread pain, more severe pain and cognitive impairment.. galectin-9 is shed by stressed neutrophils—the most abundant white blood cells—in long COVID patients. This released galectin-9 can promote chronic inflammation by affecting various immune cells.. long COVID dysregulates the production of red blood cells, which results in an abundance of immature red blood cells in the blood of these patients. Normally, immature red blood cells are present in the bone marrow but not in the blood of healthy people. It is these immature red blood cells in the blood that suppress the immune system and contribute to the elevation of artemin in the plasma of long-COVID patients."
“This is the 5th year of the pandemic in the Let It Rip Kingdom of Sweden. Everyone is constantly reinfected with the immune damaging SARS-CoV-2.
Respiratory virus/bacteria infections like Rhino/Enterovirus, Adenovirus, Mycoplasma pneumoniae or Pertussis are skyrocketing.
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“Long COVID’ affects nearly one in five adults who have had coronavirus disease 2019 (COVID-19), yet the mechanisms underlying this disorder remain poorly understood. In a new study, Cheong et al. show that the epigenetic and transcriptional state of myeloid immune cells and their progenitors are durably altered in patients following severe COVID-19.”
“Long COVID, or post-acute COVID syndrome (PACS), is now estimated to occur in 19% of adults having presented with COVID-19.. PACS is believed to be caused by immunological changes that persist after acute infection. Furthermore, it is now increasingly recognized that these changes include not only those in the adaptive immune system, such as production of autoantibodies or autoreactive T cells due to molecular mimicry, but also those in the innate immune system.. A new study by Cheong et al. in Cell reveals crucial differences in the transcriptional and epigenetic state of innate immune cells and their progenitors [among PASC patients].. the study team demonstrated that myeloid cells and hematopoietic progenitor cells harbored transcriptional and chromatin accessibility changes that did not return to baseline even 1 year after acute SARS-CoV-2 infection. These data provide powerful evidence that persistent changes (i.e., trained immunity) may underlie PACS..”
Your immune system is a factory 🧵
T-cells are the essential workers.
SARS-CoV-2 -19 is a hacker that doesn't just disrupt operations from the outside.
It infiltrates the system and systematically lays off the workers (T-cells).
“Conclusion Tuberculosis after recovering from COVID-19 is becoming more common, potentially leading to a TB outbreak in the post-COVID-19 era. The immunosuppressive nature of the disease and its treatment modalities may contribute to post COVID-19 TB.”
