Scientist surprised by discovery of '99%' effective, cheap COVID treatment

[Elderberry]

WND by Art Moore 12/30/2021

University of Florida researcher tells WND people already reporting results from Benadryl

The scientist who combined two widely available over-the-counter compounds that inhibited the novel coronavirus by 99% in early tests told WND he's hopeful his treatment will be available "within months."

"An FDA-approved treatment could be in sight within months if pharmaceutical companies utilize existing clinical trial resources," said Dr. David Ostrov in an email interview with WND.
Dr. David Ostrov, professor Professor in the Department of Pathology, Immunology and Laboratory Medicine at the University of Florida College of Medicine

Dr. David Ostrov, associate professor in the Department of Pathology, Immunology and Laboratory Medicine at the University of Florida College of Medicine

Ostrov, an immunologist and associate professor in the University of Florida College of Medicine’s department of pathology, immunology and laboratory medicine, combined diphenhydramine, which is marketed as Benadryl, and lactoferrin, a protein in milk, as WND reported in December.

"My prediction is that antiviral drug combinations, such as diphenhydramine and lactoferrin, will provide a similar level of benefit as Regeneron monoclonal antibodies, Pfizer and Merck antivirals, at less than 1/100 the cost of those therapies," he told WND

More: https://www.wnd.com/2021/12/scientist-surprised-discovery-99-effective-cheap-covid-treatment/

[catfish1957]

 

. 50 cents a pill

4 cents a pill

That scream your hear is the collective panic from Pharma CEO's.

[Wingnut]

. 50 cents a pill

4 cents a pill

That scream your hear is the collective panic from Pharma CEO's.

When I caught the Kung Fu flu this past summer I had been taking Benadryl for a allergies when I got sick.  I had a very mild case.  Maybe it was less severe because of the diphenhydramine in those tabs and in the day and night time Nyquil cold and flu liquid I was taking?   

[Elderberry]

Highly Specific Sigma Receptor Ligands Exhibit Anti-Viral Properties in SARS-CoV-2 Infected Cells

MDPI  Journals Pathogens Volume 10 Issue 11 10.3390/pathogens10111514

https://www.mdpi.com/2076-0817/10/11/1514/htm

Abstract

(1) Background: There is a strong need for prevention and treatment strategies for COVID-19 that are not impacted by SARS-CoV-2 mutations emerging in variants of concern. After virus infection, host ER resident sigma receptors form direct interactions with non-structural SARS-CoV-2 proteins present in the replication complex. (2) Methods: In this work, highly specific sigma receptor ligands were investigated for their ability to inhibit both SARS-CoV-2 genome replication and virus induced cellular toxicity. This study found antiviral activity associated with agonism of the sigma-1 receptor (e.g., SA4503), ligation of the sigma-2 receptor (e.g., CM398), and a combination of the two pathways (e.g., AZ66). (3) Results: Intermolecular contacts between these ligands and sigma receptors were identified by structural modeling. (4) Conclusions: Sigma receptor ligands and drugs with off-target sigma receptor binding characteristics were effective at inhibiting SARS-CoV-2 infection in primate and human cells, representing a potential therapeutic avenue for COVID-19 prevention and treatment.

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 2.3. Synergistic Antiviral Activity by Combining a Sigma Receptor Ligand with Lactoferrin

The antihistamine diphenhydramine, with on-target binding to the Histamine-1 receptor, has known off-target effects at the sigma-1 receptor [27]. Diphenhydramine was recently shown to inhibit SARS-CoV-2 infectivity and the calculated EC50 for SARS-CoV-2 by plaque reduction assay was 17.4 μg/mL (59.6 μM). This drug is safe, well-characterized, and widely available and so highly relevant in the search for COVID therapeutics. We investigated the ability of diphenhydramine to inhibit SARS-CoV-2 induced cytotoxicity and found an EC50 of 122.0 μg/mL (418 μM; Figure 8A,B), about 7 times higher than that found in the plaque reduction assay, similar to our findings with AZ66. We hypothesized that diphenhydramine could be combined with structurally distinct antiviral agents (binding other receptors, not sigma) to reduce its EC50 for antiviral activity against SARS-CoV-2.



Figure 8. Combinations of diphenhydramine and lactoferrin exhibit synergy against SARS-CoV-2. (A), Vero E6 cells were treated with diphenhydramine (DPH) at various concentrations without (black bars) or with SARS-CoV-2 at MOI 0.2 (gray bars) and cytotoxicity was measured by LDH release. (B), The EC50 (white circles) and CC50 (black circles) curves were determined by non-linear regression. The EC50 of diphenhydramine alone was 122 μg/mL. (C), Vero E6 cells were treated with diphenhydramine at various concentrations and lactoferrin (LFN) at 400 μg/mL without (black bars) or with SARS-CoV-2 at MOI 0.2 (gray bars) and cytotoxicity was measured by LDH release. (D), The EC50 (white circles) and CC50 (black circles) curves were determined by non-linear regression. The EC50 of diphenhydramine with 400 μg/mL of lactoferrin was 54.25 μg/mL. (E), The EC50 curves of DPH (white circles), LFN (black diamonds), and DPH+LFN (black squares) are shown on the same graph to compare effect of LFN on DPH EC50. (F), Measurement of viral genome equivalents by RT-qPCR of the SARS-CoV-2 N-protein gene demonstrate the ability of DPH+LFN to inhibit replication by almost 3-logs. *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001; ns, not significant.

More at link.

[catfish1957]

Highly Specific Sigma Receptor Ligands Exhibit Anti-Viral Properties in SARS-CoV-2 Infected Cells

MDPI  Journals Pathogens Volume 10 Issue 11 10.3390/pathogens10111514

Don't have the time or energy to make the pharmaceutical dose conversions, but apparent since the study effectiveness is in micrograms per milliliter, this must be some kind of compounded product blend.  Or for the laymen....  So much for home remedies at this point.

[Elderberry]

Lactoferrin as potential preventative and adjunct treatment for COVID-19

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7390755/

Abstract

The coronavirus disease 2019 (COVID-19) pandemic is rapidly advancing across the globe despite drastic public and personal health measures. Antivirals and nutritional supplements have been proposed as potentially useful against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the novel coronavirus that causes COVID-19, but few have been clinically established. Lactoferrin (Lf) is a naturally occurring, non-toxic glycoprotein that is orally available as a nutritional supplement and has established in vitro antiviral efficacy against a wide range of viruses, including SARS-CoV, a closely related coronavirus to SARS-CoV-2. Furthermore, Lf possesses unique immunomodulatory and anti-inflammatory effects that may be especially relevant to the pathophysiology of severe COVID-19 cases. Here we review the underlying biological mechanisms of Lf as an antiviral and immune regulator, and propose its unique potential as a preventative and adjunct treatment for COVID-19. We hope that further research and development of Lf nutritional supplementation would establish its role for COVID-19.

2.1. Lactoferrin as a broad-spectrum antiviral agent

The antiviral activity of Lf was first demonstrated in mice infected with a polycythemia-inducing strain of the Friend virus complex in the 1980s [10]. Since the 1990s, the list of Lf-susceptible pathogenic human viruses found to be inhibited by Lf have expanded to include naked and enveloped viruses as well as DNA and RNA viruses (Table 1 ), including cytomegalovirus, herpes simplex virus, human immunodeficiency virus (HIV), rotavirus, poliovirus, respiratory syncytial virus, hepatitis B virus, hepatitis C virus (HCV), parainfluenza virus, alphavirus, hantavirus, human papillomavirus, adenovirus, enterovirus 71, echovirus 6, influenza A virus and Japanese encephalitis virus, with in vitro EC50 values (half maximal effective concentration) generally in the micromolar range [11,12]. Particularly relevant to the current review is the ability of Lf to inhibit pseudotyped SARS-CoV with a 50% inhibitory concentration (IC50) of 0.7 μM [13] since it is the human coronavirus that is most closely related to SARS-CoV-2, which causes COVID-19.

Besides reducing viral entry, Lf can also suppresses virus replication after the virus enters the cell, as in the case of HIV [18]⁠. Thereafter, Lf can also exert an indirect antiviral effect on immune cells that play a crucial role in the early stages of viral infection.

In human oral supplementation studies against pathologic viruses, Lf given in the range of 100–1000 mg/day in humans was found to reduce the incidence of colds [19] and cold-like symptoms [20] as well as to ameliorate rotaviral gastroenteritis [21]. In HCV patients, a randomised controlled study involving 111 patients receiving Lf versus no Lf along with standard anti-HCV drugs demonstrated a significant decrease in HCV viral titres and sustained virological response in the Lf group [22].

2.2. Lactoferrin as an immunomodulatory and anti-inflammatory agent

Lf is a unique multifunctional moiety that is not only a broad-spectrum antiviral but also has immunomodulatory [23] and anti-inflammatory [24] actions that may play a role in the pathophysiology of severe infections. The key immunomodulatory role of this protein stems from its unique potential to maintain immune and physiological homeostasis and to limit tissue damage by modulation of cytokines, chemokines and cell surface receptors involved in cascades of signalling pathways [25]. The myriad of biological pathways of control and feedback interactions with Lf has been extensively reviewed [26]. Specific examples of the balancing and restorative roles of Lf are perhaps illustrated in the context of systemic inflammatory response syndrome (SIRS), which describes the complex physiological response to severe insults such as sepsis as defined by a consensus conference in 1991 [27]. An updated and overlapping concept of ‘cytokine storm’ similarly reflects hyperinduction of inflammatory responses resulting from unchecked immune activation [28], which Kruzel's group and others have proposed Lf might treat [25].

More at link.