: Before we really embark on answering this question, lets first us look at what happened in the early part of the pandemic. We had to endure an constant onslaught of stupid online fake news from conspiracy theories that 5G caused COVID-19 (we do believe that 5G can cause other health issues but not COVID-19 please!), that COVID-19 disease is not real, there are some crazy plans by Bill Gates who has a fetish to vaccinate people in order control them or Dr Fauci indirectly created this pathogen (hmm!...) , that the virus was man made in a lab (we have now decided to keep an open mind on this now after studying the processes involved in virus passaging) to even more dangerous claims that drinking bleach could help cure the disease to claims that wearing mask does not help etc. Most of these fake news were perpetrated by fans of Trump who can be described as lower income rural semi-educated white Caucasians. Some of the more real stupid fake cures or voodoo medicine promoted online were by scammers from certain African countries including the Nigerians.
On the other had we also had so called supposedly credible figures like the WHO disseminating misinformation and fake news such like the virus was not transmissible between human, or that the virus was not airborne etc, and we had lots of American so called virologist saying that the SARS-CoV-2 coronavirus was not mutating or if it did it would be weakened etc.
Off course the more elaborate hoaxes and scams were by the pharmaceutical companies along with the Trump administration and clandestine groups of billionaires including a group as reported by American media called the ‘Scientists to Stop Covid-19’ who are basically greedy charlatans along with the support of American social media and American mainstream media. Hence we had the hydroxychloroquine saga, the remdesivir scams, tocilizumab (this fortunately died a premature death) and soon Regeneron.(latest is that they have stopped the Regeneron trials for severe COVID-19 patients. Most of these pharma scams were glorified or sanctioned by fact checkers online and also by American media and social media platforms!
We must also not also forget the teratogenic drug favipiravir scam by the Chinese and Japanese or the Thai doctors and the local health authorities who said that they invented a treatment protocol for COVID-19 using oseltamivir and lopinavir/ritonavir!
But at the same time we also have to note that we also had many interesting studies that showed the effects that various supplements and also cheap generic drugs that could be repurposed to treat certain aspects of the COVID-19 disease as adjuvants or even by themselves. Unfortunately many of these were often deemed as fake news or misinformation by so called bastard American, Indian or Italian unqualified fact-checkers and also by numerous American owned media and social media platforms. Interestingly these are the very same countries where masses are getting inflicted by the SARS-CoV-2 coronavirus and many are dying and from the way things look, it is going to get worse for these countries.
Many of these supplements, herbs and generic drugs that could help treat COVID-19 were quietly placed in the backburners and never explored or studied again as a result of concerted efforts by the greedy pharma companies and also corrupted governments including the Trump administration.&l
Even at one stage when Vitamin D was proposed as playing a role in COVID-19 , there were some bastard fact checkers that claimed that this was fake although now numerous studies have showed otherwise. The public should identify and locate some of these unscrupulous individuals who were most probably paid by the big pharma companies and take relevant actions against them. (Thailand Medical News is in the midst of identifying and tracing details of numerous of these fact checkers, so called science writers and also so called researchers and publishing their details online as they need to be ostracized by society)
Another victim was copper supplements. When the possibility that copper supplements could help in COVID-19, it was immediately shot down and labeled as fake news by again certain bastards without giving it an opportunity to be explored or studied further.
However fortunately once again the interest in copper has popped up after certain studies also showed its efficacy as a material for disinfection against the SARS-CoV-2 in environment settings.
In terms as an oral supplement, there are no studies that are conclusive to date as most were involving observational clinical trials using copper supplements along with other drugs to treat COVID-19. https://iv.iiarjournals.org/content/34/3_suppl/1567.full
One interesting clinical trial that was surprisingly conducted in India showed that copper supplements and resveratrol reduced mortality rates in COVID-19 patients. (The results were a thousand times better than the U.S.FDA’s and Trump’s remdesivir!) https://www.medrxiv.org/content/10.1101/2020.07.21.20151423v1
Another study explored using organometallics such as copper to possible treat COVID-19. https://chemrxiv.org/articles/preprint/In_Search_for_Effective_and_Safe_Drugs_Against_SARS-CoV-2_Part_II_the_Role_of_Selected_Salts_and_Organometallics_of_Copper_Zinc_Selenium_and_Iodine_Food_Supplements/12234743/1
Copper has many interesting properties as an antiviral agent and more detailed studies are warranted to explore this.
Researchers from Canada, Finland, India and Norway wrote a piece in the journal: Medial Hypothesis, are calling for the study of copper supplements to help treat COVID-19 as an adjuvant. https://www.sciencedirect.com/science/article/pii/S0306987720308136?via%3Dihub
Copper is an essential trace dietary mineral present almost in all living organisms. Copper can boost the host's immune system response against pathogens, exhibiting strong antibacterial, antifungal, antiviral and anti-inflammatory effects. https://link.springer.com/article/10.1007%2Fs00705-008-0154-2
A study from the US National Institutes of Health (NIH) showed that SARS-CoV-2 virus survives no more than 4 h on copper surfaces compared to up to 24 h on cardboard, ≈48 h on stainless steel and ≈72 h on plastic. The same study showed that SARS-CoV-1 survives no more than 8 h on copper surfaces compared to up to 24 h on cardboard, ≈48 h on stainless steel and ≈72 h on plastic. The pathogenic human coronavirus 229E (HuCoV-229E) was rapidly inactivated on a range of copper alloys within <40 min on Cu brasses and within 120 min on Cu/Zn brasses, suggesting a concentration-response relationship https://www.nejm.org/doi/full/10.1056/nejmc2004973
Exposure to copper resulted in un-reversed damage in virus morphology (i.e.
envelope and surface spikes) and destruction of the viral genomes. Another study revealed that the application of the metal catalyst Cu/Al2O3 to surfaces for 5-20 min can destroy the replication and propagation abilities of SARS-CoV. https://mbio.asm.org/content/6/6/e01697-15.short
Copper's potential mechanism of action against viruses has been described in the numerous literatures (see above). These effects are usually concentration and time-dependent. There are mainly three mechanisms by which copper acts: (A) it damages virus membranes and “envelopes” and can destroy the DNA or RNA of the viruses, (B) it generates reactive oxygen species (ROS) that can kill the virus and, (C) it interferes with proteins that operate important functions for the virus. Sagripanti et al.
in 1993 demonstrated that Cu2+ resulted in 99% inactivation of viruses in vitro
after 30 min. https://aem.asm.org/content/59/12/4374.abstract?ijkey=c922783ce4ffbc00e26bd5513c75709d93115132&keytype2=tf_ipsecsha
Enveloped viruses were more sensitive to Cu2+ inactivation than the non-enveloped ones. The presence of RNA or lipid may render the virus particle more sensitive to inactivation by Cu2. It has been shown that Cu2+ can inhibit RNA polymerase activity by more than 60%, with copper exhibiting the strongest effect compared to other metal ions. The biological activity of these metallo-peptide drugs appears to be higher when copper is bound to a chelating amino acid or acetylacetonate. https://www.sciencedirect.com/science/article/abs/pii/S0010854517306008
Copper may also have a role in the immune system response to inflammation. In inflammatory conditions, subjects exhibited higher mean serum copper concentrations related to disease activity. Furthermore, liver copper levels were increased in adjuvant-induced arthritis in rats during the inflammatory process. https://link.springer.com/article/10.1007/BF01969106
A past study demonstrated that elevated IL-6 levels resulted in increased levels of ceruloplasmin, the major copper-carrying protein in the blood. https://bmcbiochem.biomedcentral.com/articles/10.1186/s12858-017-0076-2
Hence, the increase in copper levels could be related to the body's physiological reaction to fight inflammation. https://link.springer.com/article/10.1007/BF01969106
In addition, the inflammatory disease may be the result of insufficient hepatic copper repositories that cannot support an anti-inflammatory response. https://www.jrheum.org/content/31/8/1551.abstract?ijkey=ae180c61d563c958d5065cc59b0ce2c3c430d657&keytype2=tf_ipsecsha
Ceruloplasmin null (Cp−/−) and wild-type (WT) mice with induced experimental colitis survived for 14 days and 30 days respectively. https://gut.bmj.com/content/62/2/209.abstract?ijkey=6b4c735ec788ae2f54babca440d493ebf5bb7bb3&keytype2=tf_ipsecsha
Cp−/− mice TNFα, KC and MCP-1 levels were significantly elevated compared to those in the MT type, suggesting that ceruloplasmin expression defects may influence inflammation onset or progression.
In vitro studies have shown that ceruloplasmin may have a pathophysiological role in inflammatory diseases, acting as a physiologic inhibitor of myeloperoxidase (MPO). https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1365-2249.1997.d01-992
Interestingly another study in a crescentic glomerulonephritis (Crgn) animal model showed the down-regulation of ceruloplasmin by RNA interference (RNAi), decreased markers of glomerular proinflammatory macrophage activation and suppressed a physiological response. https://www.genetics.org/content/206/2/1139.abstract?ijkey=9e78c3c88ef890efcdbde6ee51b65ada5cc32c66&keytype2=tf_ipsecsha
Exogenous copper decreased the formation of systemic lupus erythematosus (SLE) cells in rats with a hydralazine induced collagen disease. Differences in inflammatory response were observed in rats fed with copper supplemented diet compared to standard diet. The latter presented significantly lower SOD anti-oxidative activity. https://www.sciencedirect.com/science/article/abs/pii/S0232151385800074
In addition to ceruloplasmin activity, copper chelation has been found to affect proteins involved in Fe metabolism, at the mRNA level, and in inflammatory diseases. Since inflammatory diseases and viral infections share the same inflammation signalling pathways, it could be inferred that exogenously administered copper may have anti-inflammatory effects in human viral infections, including COVID-19. https://bmcbiochem.biomedcentral.com/articles/10.1186/s12858-017-0076-2
It was found that in acute inflammatory or infectious events as well as in inflammatory diseases, such as chronic cardiac disease, chronic kidney disease and inflammatory bowel disease, patients present high serum ferritin levels and iron deficiency with adverse clinical consequences. https://www.hindawi.com/journals/ijcd/2018/9394060/
Ceruloplasmin is responsible for the reoxidation of Fe(II) to Fe(III), which is followed by loading of Fe(III) onto transferrin for systemic distribution to other sites. During inflammation, hepcidin levels increase in response to an IL-6 increase, causing degradation of the iron transporter ferroportin and reducing iron efflux from hepatocytes, enterocytes and splenic macrophages . This leads to a disruption in iron homeostasis, excess of iron stores (i.e.
ferritin) and reduction in iron availability. In vitro
and in vivo
evidence have suggested that ceruloplasmin may have a role in iron trafficking across the enterocyte during inflammation, participating in host defence and balancing of ferritin levels .
Significantly In severe COVID-19 cases, high serum ferritin levels have been reported. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7131471/
In viral infection, autophagy has been demonstrated to have an antiviral response to viral oxidative stress. Autophagy enables cells to survive stress from an external environment attack, like a viral infection. Induction of autophagy, marked by autophagic vacuoles formation that degrades the viral invading proteins, limits the viral infection. It has been demonstrated that copper induces autophagy and apoptosis and is correlated with the formation of autophagic vacuoles maintaining the cell's anti-viral defence (80, 81). https://www.sciencedirect.com/science/article/abs/pii/S0147651319310413
These data findings, linking copper with autophagy and vacuoles formation, support further studies of copper as a candidate for the treatment of viral infections. The copper/autophagy interconnection opens potential therapeutic application studies and clinical development of copper to target COVID-19 infection.
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