Authors: Christopher G. Thomas, 301-496-5751, firstname.lastname@example.org
Results from a study of 19 deceased patients suggests brain damage is a byproduct of a patient’s illness.
In an in-depth study of how COVID-19 affects a patient’s brain, National Institutes of Health researchers consistently spotted hallmarks of damage caused by thinning and leaky brain blood vessels in tissue samples from patients who died shortly after contracting the disease. In addition, they saw no signs of SARS-CoV-2 in the tissue samples, suggesting the damage was not caused by a direct viral attack on the brain. The results were published as a correspondence in the New England Journal of Medicine.
“We found that the brains of patients who contract infection from SARS-CoV-2 may be susceptible to microvascular blood vessel damage. Our results suggest that this may be caused by the body’s inflammatory response to the virus,” said Avindra Nath, M.D., clinical director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We hope these results will help doctors understand the full spectrum of problems patients may suffer so that we can come up with better treatments.”
For More Information: https://www.nia.nih.gov/news/nih-study-uncovers-blood-vessel-damage-and-inflammation-covid-19-patients-brains-no-infection
Authors: Jia Yu, Xuan Yuan, Hang Chen, Shruti Chaturvedi, Evan M. Braunstein, Robert A. Brodsky
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly contagious respiratory virus that can lead to venous/arterial thrombosis, stroke, renal failure, myocardial infarction, thrombocytopenia, and other end-organ damage. Animal models demonstrating end-organ protection in C3-deficient mice and evidence of complement activation in humans have led to the hypothesis that SARS-CoV-2 triggers complement-mediated endothelial damage, but the mechanism is unclear. Here, we demonstrate that the SARS-CoV-2 spike protein (subunit 1 and 2), but not the N protein, directly activates the alternative pathway of complement (APC). Complement-dependent killing using the modified Ham test is blocked by either C5 or factor D inhibition. C3 fragments and C5b-9 are deposited on TF1PIGAnull target cells, and complement factor Bb is increased in the supernatant from spike protein–treated cells. C5 inhibition prevents the accumulation of C5b-9 on cells, but not C3c; however, factor D inhibition prevents both C3c and C5b-9 accumulation. Addition of factor H mitigates the complement attack. In conclusion, SARS-CoV-2 spike proteins convert nonactivator surfaces to activator surfaces by preventing the inactivation of the cell-surface APC convertase. APC activation may explain many of the clinical manifestations (microangiopathy, thrombocytopenia, renal injury, and thrombophilia) of COVID-19 that are also observed in other complement-driven diseases such as atypical hemolytic uremic syndrome and catastrophic antiphospholipid antibody syndrome. C5 inhibition prevents accumulation of C5b-9 in vitro but does not prevent upstream complement activation in response to SARS-CoV-2 spike proteins.
For More Information: https://ashpublications.org/blood/article/136/18/2080/463611/Direct-activation-of-the-alternative-complement
Authors: Yuichiro J. Suzuki,a,⁎ Sofia I. Nikolaienko,b Vyacheslav A. Dibrova,b Yulia V. Dibrova,b Volodymyr M. Vasylyk,c Mykhailo Y. Novikov,d Nataliia V. Shults,a and Sergiy G. Gychkab
Currently, the world is suffering from the pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that uses angiotensin-converting enzyme 2 (ACE2) as a receptor to enter the host cells. So far, 60 million people have been infected with SARS-CoV-2, and 1.4 million people have died because of COVID-19 worldwide, causing serious health, economical, and sociological problems. However, the mechanism of the effect of SARS-CoV-2 on human host cells has not been defined. The present study reports that the SARS-CoV-2 spike protein alone without the rest of the viral components is sufficient to elicit cell signaling in lung vascular cells. The treatment of human pulmonary artery smooth muscle cells or human pulmonary artery endothelial cells with recombinant SARS-CoV-2 spike protein S1 subunit (Val16 – Gln690) at 10 ng/ml (0.13 nM) caused an activation of MEK phosphorylation. The activation kinetics was transient with a peak at 10 min. The recombinant protein that contains only the ACE2 receptor-binding domain of the SARS-CoV-2 spike protein S1 subunit (Arg319 – Phe541), on the other hand, did not cause this activation. Consistent with the activation of cell growth signaling in lung vascular cells by the SARS-CoV-2 spike protein, pulmonary vascular walls were found to be thickened in COVID-19 patients. Thus, SARS-CoV-2 spike protein-mediated cell growth signaling may participate in adverse cardiovascular/pulmonary outcomes, and this mechanism may provide new therapeutic targets to combat COVID-19.
Author: Dr. Charles Hoffe
in a Coronavirus, that spike protein becomes part of the viral capsule. In other words, the cell wall around the virus, called the viral capsule. But it’s not in the virus. It’s in your cells. So it therefore becomes part of the cell wall of your vascular endothelium. Which means that these cells that line your blood vessels, which are supposed to be smooth so that blood flows smoothly, now have these little spikey bits sticking out.
So it is absolutely inevitable that blood clots will form. Because your blood platelets circulate around in your blood vessels. And the purpose of blood platelets is to detect a damaged vessel and block that vessel to stop bleeding. So when the platelet comes through the capillary, it suddenly hits all these all these Covid spikes that are jutting into the inside of the vessel, it is absolutely inevitable that a blood clot will form to block that vessel. That’s how platelets work.
For More Information: https://citizenfreepress.com/breaking/dr-charles-hoffe-issues-vaccine-warning/
Authors: Richard N. Fogoros, MD
The D-dimer test is a blood test that indicates whether blood clots are being actively formed somewhere within a person’s vascular system. This test is most often helpful in the diagnosis of pulmonary embolus and deep vein thrombosis, but it can also be useful in diagnosing other medical conditions in which blood clots play a role.
However, there are limitations to the D-dimer test, and it can be tricky to evaluate the results. In order to avoid being misled by it, doctors need to make sure they are using this test at the appropriate times and must take due care in interpreting the results.
For More Information: https://www.verywellhealth.com/d-dimer-test-4173338
Whether it’s strange rashes on the toes or blood clots in the brain, the widespread ravages of COVID-19 have increasingly led researchers to focus on how the novel coronavirus sabotages blood vessels.
As scientists have come to know the disease better, they have homed in on the vascular system — the body’s network of arteries, veins and capillaries, stretching more than 60,000 miles — to understand this wide-ranging disease and to find treatments that can stymie its most pernicious effects.
Some of the earliest insights into how COVID-19 can act like a vascular disease came from studying the aftermath of the most serious infections. Those reveal that the virus warps a critical piece of our vascular infrastructure: the single layer of cells lining the inside of every blood vessel, known as the endothelial cells or simply the endothelium.