Fauci knows that N-acetylcysteine therapy works
NAC, which has been used clinically to treat acetaminophen toxicity, is believed to act by increasing the intracellular level of GSH (22, 23). Cellular GSH levels may also be increased by administration of GSH monoester (GSE), a readily transported derivative of GSH, which also protects very effectively against acetaminophen toxicity. Although GSH is not transported intact into cells, it may be degraded into its constituent amino acids, which after transport are used for the synthesis of GSH. These findings suggested that cellular reducing systems may be involved in preventing HIV activation and thus in maintaining a state of viral latency. We therefore investigated the hypothesis that GSH, GSH derivatives, or NAC may inhibit the induction of virus expression in our model system of chronic HIV infection.
NAC produced >90% suppression of the HIV E mRNA level in both PMA- and TNF-a-stimulated Ul cells.
In contrast, GSH and GSE reduced the HIV mRNA level only 10-15%. Although it has been assumed that NAC exerts some of its effects by increasing intracellular GSH (19, 23), our findings suggest that the mechanisms of NAC mediated inhibition of HIV expression may be complex and involve, for example, a more efficient rate of internalization, an extracellular effect, or an effect on intracellular proteins.
Other thiols, which are not directly used for GSH synthesis, have been reported to suppress HIV replication in acute systems. Such thiols [including penicillamine (35, 36), and 2,3-dimercapto-1- 0.0 0.3 0.6 0.9 1.2 1.5 propanol (37)], as well as ascorbate (vitamin C) (38) could act to spare cellular GSH; the thiols might liberate GSH moieties from mixed disulfide linkages with proteins.
Our observation that GSH, GSE, and NAC can suppress the induction of HIV expression in vitro by TNF-a and IL-6 leads to the hypothesis that these agents may have similar effects in vivo and therefore that the administration of these or similar agents may have therapeutic value in HIV-infected patients.
Such therapy may be effective in limiting progression of the disease process, which, by a presently unknown mechanism, produces a striking decrease in the level of a major cellular antioxidant.
This “a presently unknown mechanism, produces a striking decrease in the level of a major cellular antioxidant” is the toxicity of injections (vaccines) and other toxins.
The mechanism is known and is very simple, it is called oxidative stress, leading to oxidative damage caused by free oxygen radicals (reactive oxygen species).
This is what “Covid” and vaccine injury is really all about. It is poisoning caused by the toxicity of nanotechnology and other substances or radiation that cause acute oxidative stress.
NAC and other thiols are one way out of the impasse....
Fauci knows this.
https://www.bcm.edu/news/covid-19-patients-have-increased-oxidative-stress-oxidant-damage-and-glutathione-deficiency COVID-19 patients have increased oxidative stress, oxidant damage, and glutathione deficiency | BCM
“We were surprised to see that the COVID-19 patients in the 21 to 40 and the 41 to 60 groups had much less glutathione and more oxidative stress than the corresponding age groups without COVID-19,” Sekhar said. “We knew that healthy people without COVID-19 above the age of 60 years tend to be glutathione-deficient and have elevated oxidative stress. However, when the 60-plus age group gets COVID-19, their glutathione levels were much lower and oxidative stress was much higher than those of a similar age but without COVID-19.”
Oxidative stress results from the accumulation of free radicals, highly reactive molecules that can damage cells, membranes, lipids, proteins and DNA. Cells in the body make glutathione to protect themselves from oxidative stress. When cells fail to neutralize free radicals, harmful cellular damage can occur and potentially affect many physiological processes.
“Our previous work has shown that increased levels of oxidative stress and reduced glutathione are not only present in older people, but also in people with HIV, a viral infection, and in patients with diabetes. We also found that supplementing GlyNAC, a combination of glutathione precursors, improved these defects in all these populations,” Sekhar said.
In addition, Sekhar’s work revealed that supplementing GlyNAC to older people and HIV-patients reversed other abnormalities including inflammation, endothelial dysfunction, insulin resistance, and improved muscle strength, exercise capacity, cognitive decline, gene-damage, and body composition. Some of these defects also have been reported in patients with COVID-19.
https://web.archive.org/web/20190303115754/http://theperthgroup.com:80/HIV/CellOxFinal.pdf
“To our surprise, given the relatively short time (8-32 weeks) that NAC was administered, we found that NAC ingestion was associated with substantially longer survival…The association of prolonged survival in the oral administration of NAC in this study is very dramatic…[our study] established GSH as a key determinant of survival in HIV disease”.3
According to these researchers their study “established GSH deficiency as a key determinant of survival in HIV disease”. They further commented “Therefore, our findings basically argue for the initiation of a placebo-controlled trial designed specifically to determine the therapeutic value of NAC in AIDS and/or that of other GSH-replenishing drugs. Since NAC is nontoxic and could be used where medical services are limited, our findings indicate that such a trial should be initiated as soon as possible. Other pharmaceuticals that replenish GSH should also be tried for the same purpose. In any event, the poor survival that we have demonstrated in GSH-depleted subjects with AIDS underscores the importance of finding ways to replenish GSH in these individual and ways to prevent GSH depletion in the disease…
Not only did Montagnier forget or ignore our group and our explicit evidence that cellular oxidation plays a “fundamental role in illness”, but, like the Herzenbergs, he forgot or ignored our list of oxidising agents to which the AIDS-risk patients are exposed. And that such exposures occur long before the patients develop HIV and opportunistic infections. Montagnier also seems unaware that it is oxidation which leads to the opportunistic infections. After all, it is his compatriot Pasteur who taught us “Bernard was right; the pathogen is nothing; the terrain is everything”.
We have also directly challenged Montagnier to defend “HIV” and the HIV theory and refute our theory in two scientific publications in 200444 and 2006.45 Although this matter was now in the public domain again Montagnier did not respond. Remarkably nowadays Montagnier accepts that in Africa the cause of AIDS is oxidation and advocates treating AIDS patients with antioxidants.46, 47 If Montagnier accepts oxidation as the cause of AIDS in Africa then why not in the other risk groups where individuals are exposed to strong oxidants?14 Nonetheless, since he accepts that in Africans (a) AIDS is due to oxidation; (b) oxidation is due to malnutrition (poverty48); it follows that the cause of AIDS in the vast majority of people is not HIV. This being the case, why not in the remaining minority?
https://pmc.ncbi.nlm.nih.gov/articles/PMC10696844/ Severity of oxidative stress as a hallmark in COVID-19 patients - PMC
https://pmc.ncbi.nlm.nih.gov/articles/PMC9024445/ Oxidative Stress and Inflammatory Status in COVID-19 Outpatients: A Health Center-Based Analytical Cross-Sectional Study - PMC
In general, viruses cause an imbalance in the cellular redox environment, which, depending on the virus and the cell, can result in different responses, e.g., cell signaling and antioxidant defenses [46]. When a virus enters the human body under oxidative stress conditions, the levels of antioxidant biomarkers increase to protect against oxidative compounds [31]. On the other hand, existing evidence shows that the adequate intake of specific foods and nutrients can effectively improve the inflammatory state and oxidative stress [47]. These concepts emphasize the importance of the relationship between nutrition, inflammation, oxidative stress, and the body’s response to viral infections. Consequently, the poor nutritional status of zinc is associated with an increased risk of COVID-19 disease, as shown in our recent study [48].
https://pmc.ncbi.nlm.nih.gov/articles/PMC9100929/ Oxidative Stress and Hyper-Inflammation as Major Drivers of Severe COVID-19 and Long COVID: Implications for the Benefit of High-Dose Intravenous Vitamin C - PMC
CONCLUSION AND OUTLOOK
As oxidative stress plays a pivotal role in the pathophysiology of COVID-19 as well as in Long COVID, the therapeutic use of antioxidants in affected patients should be further addressed by RCTs. This is underlined by 6 small studies demonstrating hypovitaminosis C in plasma or serum during acute COVID-19 (Holford et al., 2021).
In Long COVID, there are still no studies available on markers of oxidative stress and antioxidants.
The relevance of treatment duration is supported by a recent nationwide cohort study that investigated iv vitamin C in sepsis and revealed a significant reduction in mortality when applied for ≥5 days (Jung et al., 2022) ….
(From: https://fieldoffitness.com/what-are-free-radicals-and-antioxidants/)
https://pmc.ncbi.nlm.nih.gov/articles/PMC1808645/ Oxygen free radicals and systemic autoimmunity - PMC
Reactive oxygen species generated during various metabolic and biochemical reactions have multifarious effects that include oxidative damage to DNA leading to various human degenerative and autoimmune diseases….
https://pmc.ncbi.nlm.nih.gov/articles/PMC5039077/ Toxicology of Graphene-Based Nanomaterials - PMC
Thank you so much.
Great info, shared