BREAKING! University of Arkansas Discovers Unique ACE-2 Targeting Antibody That Appears Weeks After COVID-19 As Main Cause Of LONG COVID!
: The COVID-19 pandemic is an extremely dynamic event in which new and better evolving research are constantly materializing and superseding whatever we had earlier known along with the fact that there are constantly new players in the pandemic due to the variety of emerging SARS-CoV-2 variants, each with unique mutations, characteristics, pathogenesis and their own specific manner of disrupting the various cellular pathways of the human host.
Identified Antibody That Causes Long-COVID or PASC
In reality most of the COVID-19 research prior to July 2021 is actually outdated and people should be aware of companies peddling therapeutics products based on past studies be it herbal products, supplements, repurposed drugs, drugs developed prior to July 2021 and even antibody based therapeutics.
A new breakthrough study that dispels all the rubbish and sub-standard research with regards to long-COVID including nonsensical talk of various pathways being disrupted by the SARS-CoV-2 that is causing long COVID conditions etc has been finally peer reviewed and published in a credible medical journal.
Leading qualified researchers from the fields of microbiology and immunology (Readers should always be wary of research carried by so called experts who are not qualified in a particular field as has been found in many past studies!) from the University of Arkansas for Medical Sciences-USA have found that a unique antibody that targets the ACE2 receptors and enzymes materializes weeks after a person has been infected by the SARS-CoV-2 coronavirus and is deemed as recovered based on existing medical protocols.
This breakthrough findings not only explains the reasons behind Long COVID but further studies are warranted to see any possible association with the Multi-System Inflammatory Syndrome(MIS) seen in certain COVID-19 recovered children and adults.
According to the study team, “Activation of the immune system is implicated in the Post-Acute Sequelae after SARS-CoV-2 infection (PASC) commonly, referred to as Long COVID, but the specific mechanisms remain unknown. Angiotensin-converting enzyme 2 (ACE2) cleaves angiotensin II (Ang II) resulting in decreased activation of the AT1 receptor and decreased immune system activation.
The study team hypothesized that autoantibodies against ACE2 may develop after SARS-CoV-2 infection, as anti-idiotypic antibodies to anti-spike protein antibodies.
The study team tested plasma or serum for ACE2 antibodies in 67 patients with known SARS-CoV-2 infection and 13 with no history of infection. None of the 13 patients without history of SARS-CoV-2 infection and 1 of the 20 outpatients that had a positive PCR test for SARS-CoV-2 had levels of ACE2 antibodies above the cutoff threshold. In contrast, 26/32 (81%) in the convalescent group and 14/15 (93%) of patients acutely hospitalized had detectable ACE2 antibodies.
Interestingly plasma from patients with antibodies against ACE2 had less soluble ACE2 activity in plasma but similar amounts of ACE2 protein compared to patients without ACE2 antibodies. The study team measured the capacity of the samples to inhibit ACE2 enzyme activity. Addition of plasma from patients with ACE2 antibodies led to decreased
activity of an exogenous preparation of ACE2 compared to patients that did not have antibodies.
The study findings shockingly showed that many patients with a history of SARS-CoV-2 infection have antibodies specific for ACE2. Patients with ACE2 antibodies have lower activity of soluble ACE2 in plasma. Plasma from these patients also inhibits exogenous ACE2 activity.
These study findings are consistent with the hypothesis that ACE2 antibodies develop after SARS-CoV-2 infection and decrease ACE2 activity. This could lead to an increase in the abundance of Ang II, which causes a proinflammatory state that triggers symptoms of PASC.
The study findings were published in the peer reviewed journal: PLOS One https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0257016
This breakthrough study has identified a potential cause of long-lasting symptoms experienced by COVID-19 patients, often referred to as long-haulers.
Lead researcher Dr John Arthur, M.D., Ph.D., professor and chief of the Division of Nephrology in the UAMS College of Medicine, Department of Internal Medicine told Thailand Medical News, “A key component of the team's findings is an antibody that shows up weeks after an initial infection and attacks and disrupts a key regulator of the immune system.”
To date as many as 30% of COVID-19 patients experience lingering fatigue, brain fog and shortness of breath. The cause of long COVID-19 has eluded scientists, but the UAMS team's discovery sheds important new light on the molecular-level mechanisms behind it.
Dr Arthur further added, "Everything that the study team found is consistent with this antibody as the instigator of long COVID, so it's an exciting development that merits further study.”
This newly discovered antibody creates problems for the immune system by attacking the angiotensin-converting enzyme 2 (ACE2). The ACE2 enzyme helps regulate the body's response to the virus by metabolizing a peptide that activates the immune system. The attacking antibody interferes with ACE2's work, which makes the antibody a prime suspect for the long-lasting illness.
Furthermore it should be noted that as a result of ACE2 being abundant and found in many key organs and tissues in the human host, numerous medical conditions can arise as a result of attacks by this by antibody.
study team was brought together quickly this spring by the University of Arkansas Medical for Sciences (UAMS) Translational Research Institute to test the hypothesis that developed through discussions between Dr Arthur and UAMS' Dr Terry Harville, M.D., Ph.D., a professor in the Department of Pathology and medical director of the Histocompatibility and Immunogenetics Laboratories.
Immunology experts cum researchers Dr Karl Boehme, Ph.D., Dr Craig Forrest, Ph.D., and Dr Shana Owens, Ph.D., in the Department of Microbiology and Immunology developed the assay (test) used to identify the antibodies.
The study team tested plasma or serum for ACE2 antibodies in 67 patients with known SARS-CoV-2 (the virus that causes COVID-19) infection and 13 with no history of infection. In 81% of blood samples from patients in Arkansas and Oklahoma with a history of COVID-19, the samples had the antibody that attacked the ACE2.
Importantly in participants with no history of COVID-19, no antibodies were created to attack the ACE2 enzyme.
Dr Arthur added, "If we show that the whole hypothesis is right, that this interference of ACE2 really does cause long COVID, then it opens up many potential treatments. If our next steps confirm that this antibody is the cause of long COVID symptoms, there are medications that should work to treat them. If we get to that phase of research, the next step would be to test these drugs and hopefully relieve individuals of the symptoms they're having."
The extensive multidisciplinary study team besides including experts in microbiology and immunology also includes UAMS College of Medicine researchers Dr Christian Herzog, Ph.D., Department of Internal Medicine; Dr Josh Kennedy, M.D., Department of Pediatrics; and Dr Juan Liu, Ph.D., from the Department of Pathology.
Dr Arther added, "This is true team science. We put together a great group of investigators that had never worked together to produce these very exciting results."
This breakthrough study findings supersedes all previous garage spewed about Long COVID and disruptions in various identified pathways etc.
But the study team stopped short of commenting as to whether exposure to spike proteins via the COVID-19 shots would also trigger such antibodies and also cause long term health issues. This is a critical question that remains to be answered!
To date there are no known or proven therapeutic products to treat Long COVID-19. There are a lot of charlatans peddling supplements, homeopathic garbage and overpriced non-proven substandard Ayurvedic and Traditional Chinese Medications. Some even use pseudoscience to market their products or simply pay substandard Indian research teams or research teams from other third world countries to provide manipulated clinical study findings.
Thailand Medical News has to date developed a herbal tea blend to help prevent or treat the conditions of myocarditis. https://www.thailandmedical.news/news/new-therapeutic-teas-
However Thailand Medical News has entered into an agreement with a biotech company in Texas-USA and also a supplement manufacturer in Elche-Spain along with collaboration from the Northwestern University-Illinois,USA and Excelsior College-Albany-New York, USA to develop a new line of nanotechnology based phytochemical therapeutics to treat Long COVID-19. Two long COVID specialty centers in New York will also be assisting with clinical trials that will start in late October. Full details of this project will be available at the end of this month on our new site: www.longcovid.news
(Note that sometimes site work might be delayed as all this projects are basically handled by one sole person with limited resources and funds!)
For more on Long COVID
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