Covid 19: adjuvant approaches etc,

[WillBrink]

This study suggests NAC may have a direct effect on spike protein binding vs just via conversion to GSH so a potentially important finding:

cysteine: A tool to perturb SARS-CoV-2 spike protein conformation

The infection caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) resulted in a pandemic with huge death toll and economic consequences. The virus attaches itself to the human epithelial cells through noncovalent bonding of its spike protein with the angiotensin-converting enzyme-2 (ACE2) receptor on the host cell.

We hypothesized that perturbing the functionally active conformation of spike protein through reduction of its solvent accessible disulfide bond, thereby disintegrating its structural architecture, may be a feasible strategy to prevent infection. Proteomics data showed that N-acetyl cysteine (NAC), an antioxidant and mucolytic agent been widely in use in clinical medicine, forms covalent conjugates with solvent accessible cysteine residues of spike protein that were disulfide bonded in the native state. In silico analysis indicated that this covalent conjugation perturbed the stereo specific orientations of the interacting key residues of spike protein that resulted in threefold weakening in the binding affinity of spike protein with ACE2 receptor.

Antiviral assay using VeroE6 cells showed that NAC caused 54.3% inhibition in SARS-CoV-2 replication. Interestingly, almost all SARS-Cov-2 variants conserved cystine residues in the spike protein.

Our observed results open avenues for exploring in vivo pharmaco-preventive and therapeutic potential of NAC for Coronavirus Disease 2019 (COVID-19).

https://chemrxiv.org/articles/prepri...ID-19/12687923

[WillBrink]

I’d like to see the actual paper and data, but something to look file under worth looking at. It would be interesting to see what, if any, association would then exist with 25OHD levels, magnesium status, and so forth with T levels in those men, and covid complications:

Men with symptomatic Covid-19 and low testosterone are six times more likely to become severely ill and die from the disease, new research has shown.

The study, conducted by researchers at San Raffaele University Hospital in Milan, Italy, found that the lower the levels of testosterone, the higher the likelihood that male patients would need intensive care, be intubated on a ventilator and remain in hospital over a longer period.

For the study, the team compared 286 male Covid patients, who came to the emergency department, with 305 healthy male volunteers between February and May 2020.
Nearly 90 per cent of the patients had testosterone below 9.2 nanomoles per litre (nmol/l), compared to just 17 per cent of the healthy volunteers. Those with testosterone levels between 3-4 nmol/l and had mild symptoms or were admitted to hospital, while those admitted to ICU or died of the disease had just 0.7-1.0 nmol/l.

"At the start of the Covid pandemic, we were seeing far more men than women coming to hospital and suffering very severe forms of the disease. We immediately thought this might be related to male hormone levels, particularly testosterone," Professor Andrea Salonia, a specialist in urology and endocrinology at the hospital.

"But we never expected to see such a high proportion of Covid patients with these extremely low levels of testosterone, in comparison to a similar group of healthy men. The relationship is very clear: the lower the testosterone, the higher the severity of the condition and likelihood of death. I've never seen anything like it in my 25 years in the field," Salonia added.

However, since the team does not have data on the testosterone levels in the patients before they contracted Covid-19, they cannot say whether low testosterone was a pre-existing long-term condition that exacerbated the disease or whether it was caused by the SARS-COV2 virus.

"Testosterone does play a role in protecting men from disease. However, it's also possible that the virus itself is able to induce an acute reduction in testosterone levels, which then predisposes these men to a worse outcome," Salonia said.

The findings will be presented at the 2021 European Association of Urology congress (EAU21), which starts from July 8-12.-IANS


https://www.theweekendleader.com/Hea...rom-covid.html

[Disciple]

Antiviral assay using VeroE6 cells showed that NAC caused 54.3% inhibition in SARS-CoV-2 replication.

I started taking NAC in April 2020 on the recommendation of one of the Medcram videos from Dr. Roger Seheult. It seems his intuition in this case was good.

[WillBrink]

I started taking NAC in April 2020 on the recommendation of one of the Medcram videos from Dr. Roger Seheult. It seems his intuition in this case was good.

His intuition you say?

[Arik]

I started taking NAC in April 2020 on the recommendation of one of the Medcram videos from Dr. Roger Seheult. It seems his intuition in this case was good.

Did you get sick? We're you exposed to the virus? Was there an antibody test done? How do you know it did anything at all?

Sent from my moto z4 using Tapatalk

[Disciple]

His intuition you say?

I wasn't reading anything of yours at that time. Haven't you recommended the Medcram videos? Pardon me if I stumbled into a history I did not know.

Arik, I have not been sick and I was never tested. I chose to take D3, zinc, and NAC as a precaution. I cannot prove what it did or did not do. How would I?

[WillBrink]

I wasn't reading anything of yours at that time. Haven't you recommended the Medcram videos? Pardon me if I stumbled into a history I did not know.

Arik, I have not been sick and I was never tested. I chose to take D3, zinc, and NAC as a precaution. I cannot prove what it did or did not do. How would I?

I have. Lots of good intel on that page.

[WillBrink]

Potentially a very important finding, albeit preliminary data:

L-Carnitine Tartrate Downregulates the ACE2 Receptor and Limits SARS-CoV-2 Infection
Nutrients 2021, 13(4), 1297

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been responsible for one of the worst pandemics in modern history. Several prevention and treatment strategies have been designed and evaluated in recent months either through the repurposing of existing treatments or the development of new drugs and vaccines. In this study, we show that L-carnitine tartrate supplementation in humans and rodents led to significant decreases of key host dependency factors, notably angiotensin-converting enzyme 2 (ACE2), transmembrane protease serine 2 (TMPRSS2), and Furin, which are responsible for viral attachment, viral spike S-protein cleavage, and priming for viral fusion and entry. Interestingly, pre-treatment of Calu-3, human lung epithelial cells, with L-carnitine tartrate led to a significant and dose-dependent inhibition of the infection by SARS-CoV-2. Infection inhibition coincided with a significant decrease in ACE2 mRNA expression levels. These data suggest that L-carnitine tartrate should be tested with appropriate trials in humans for the possibility to limit SARS-CoV-2 infection.

Paper:

https://www.mdpi.com/2072-6643/13/4/1297/htm

[P2Vaircrewman]

I take Losartan for blood pressure along with hydrochlorothiazide. Losartan is an angiotensin II receptor blocker. Seems the research is more about starting someone with covid as treatment rather than as a prophylactic treatment before covid but I wonder if it might have a prophylactic effect.

[WillBrink]

I take Losartan for blood pressure along with hydrochlorothiazide. Losartan is an angiotensin II receptor blocker. Seems the research is more about starting someone with covid as treatment rather than as a prophylactic treatment before covid but I wonder if it might have a prophylactic effect.

Losartan and similar were being examined at one time as possible treatment options. Didn't seem to help with those already diagnosed, but I know studies are ongoing as to what/what/where such drugs may be benefit. Some info:

https://www.drugs.com/medical-answer...virus-3534166/