It should be a well-known fact amongst all the coronavirus paranoia that an effective, functional immune system means that an infection with this virus is very mild. All serious complications occur in people with poor immunity. Turmeric contains curcumin amongst other beneficial components, and these are widely recognised as being good for stimulating immune function as well as for health and vitality. There is a lot of evidence that turmeric stimulates immunity to many different viral infections. It will obviously have a similar effect on the new coronavirus and those people full of turmeric will be laughing.
It is very important to take turmeric in a form that can be metabolised and absorbed and Golden Paste in food is that. Additionally, our specially formulated, convenient products, including our Power Bars and Bites, are another option.
That this new virus has emerged is not surprising, because dense populations of carriers that allow viruses to interchange and hybridise will always continue to throw out new virions that could be very virulent. Turmeric consumption is just one action you can take to help protect yourself into the future.
To give credibility, I have summarised the take-home snippets from the listed scientific citations below that I have selected from hundreds.
1. Is a promising treatment for influenza A virus and prevents injury to virus-infected lung tissue; 1
2. Protects against enteroviral infections by decreasing replication in the intestines. curcumin treatment inhibits viral translation and increases host cell viability; 2
3. Relieves inflammation in influenza infected lungs; 3
4. Curcumin is a potent inhibitor of Epstein-Barr virus transformed lymphoblastoid cell lines (LCL) through enhanced apoptosis which is useful in immunodeficient people; 4
5. Curcumin can directly inactivate Influenza A Virus, inhibits Influenza A Virus adsorption, and replication; 5
6. Recently, curcumin's antiviral and antibacterial activity was investigated, and it was shown to act against various important human pathogens like the influenza virus, hepatitis C virus, HIV and strains of Staphylococcus, Streptococcus, and Pseudomonas; 6
7. Curcumin inhibits the infectivity of enveloped viruses; 7
8. Curcumin can suppress Hepatitis C Virus (HCV) replication. 8
1. Clin Exp Pharmacol Physiol. 2018 Jan;45(1):84-93. doi: 10.1111/1440-1681.12848. Epub 2017 Oct 3.
Curcumin ameliorates severe influenza pneumonia via attenuating lung injury and regulating macrophage cytokines production.
Han S1,2, Xu J1, Guo X1, Huang M1.
Curcumin, an active phenolic agent extract from the Curcuma longa, exhibits excellent anti-cancer, anti-inflammation, and neuroprotective effects.
We aimed to investigate the anti-influenza role of curcumin in vitro and in vivo.
The effect of curcumin on replication of influenza A virus (IAV) was examined in human lung cancer cell line A549, as well as in a mouse model.
Curcumin could inhibit IAV in vitro and alleviate the severity of the disease in the mouse after infection with IAV. The results also indicated that curcumin could trigger expression of Heme oxygenase-1 in vivo and attenuate IAV-induced injury to the lung tissue.
Furthermore, curcumin could regulate immune response following IAV infection through inhibiting production of local inflammatory cytokines.
In addition, curcumin was found to inhibit NF-κB signalling in macrophages, as well as the subsequent production of cytokines/chemokines responding to IAV infection, by enhancing IκBα and AMPK.
Our current study supports the potential of curcumin as a promising treatment against IAV infection, whose effect may be mediated by regulating immune response to prevent injury to the lung tissue.
2. PLoS One.2018 Jan 25;13(1):e0191617. doi: 10.1371/journal.pone.0191617. eCollection 2018.
Inhibition of EV71 by curcumin in intestinal epithelial cells.
Huang HI1,2,3,4, Chio CC1,3, Lin JY1,3.
EV71 is a positive-sense single-stranded RNA virus that belongs to the Picornaviridae family.
EV71 infection may cause various symptoms ranging from hand-foot-and-mouth disease to neurological pathological conditions such as aseptic meningitis, ataxia, and acute transverse myelitis.
There is currently no effective treatment or vaccine available. Various compounds have been examined for their ability to restrict EV71 replication.
However, most experiments have been performed in rhabdomyosarcoma or Vero cells. Since the gastrointestinal tract is the entry site for this pathogen, we anticipated that orally ingested agents may exert beneficial effects by decreasing virus replication in intestinal epithelial cells.
In this study, curcumin (diferuloylmethane, C21H20O6), an active ingredient of turmeric (Curcuma longa Linn) with anti-cancer properties, was investigated for its anti-enterovirus activity.
We demonstrate that curcumin treatment inhibits viral translation and increases host cell viability.
Curcumin does not exert its anti-EV71 effects by modulating virus attachment or virus internal ribosome entry site (IRES) activity.
Furthermore, curcumin-mediated regulation of mitogen-activated protein kinase (MAPK) signalling pathways is not involved.
We found that protein kinase C delta (PKCδ) plays a role in virus translation in EV71-infected intestinal epithelial cells and that curcumin treatment decreases the phosphorylation of this enzyme.
In addition, we show evidence that curcumin also limits viral translation in differentiated human intestinal epithelial cells.
In summary, our data demonstrate the anti-EV71 properties of curcumin, suggesting that ingestion of this phytochemical may protect against enteroviral infections.
3. Influenza Other Respir Viruses. 2017 Sep;11(5):457-463. doi: 10.1111/irv.12459. Epub 2017 Jul 11.
Curcumin alleviates macrophage activation and lung inflammation induced by influenza virus infection through inhibiting the NF-κB signaling pathway.
Influenza A viruses (IAV) result in severe public health problems with worldwide each year. Overresponse of immune system to IAV infection leads to complications, and ultimately causing morbidity and mortality.
Curcumin has been reported to have anti-inflammatory ability. However, its molecular mechanism in immune responses remains unclear.
We detected the pro-inflammatory cytokine secretion and nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB)-related protein expression in human macrophages or mice infected by IAV with or without curcumin treatment.
We found that the IAV infection caused a dramatic enhancement of pro-inflammatory cytokine productions of human macrophages and mice immune cells. However, curcumin treatment after IAV infection downregulated these cytokines production in a dose-dependent manner. Moreover, the NF-κB has been activated in human macrophages after IAV infection, while administration of curcumin inhibited NF-κB signaling pathway via promoting the expression of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα), and inhibiting the translocation of p65 from cytoplasm to nucleus.
In summary, IAV infection could result in the inflammatory responses of immune cells, especially macrophages. Curcumin has the therapeutic potentials to relieve these inflammatory responses through inhibiting the NF-κB signalling pathway.
4. J Surg Res.1999 Nov;87(1):1-5.
Enhanced apoptosis mediates inhibition of EBV-transformed lymphoblastoid cell line proliferation by curcumin.
Ranjan D1, Johnston TD, Reddy KS, Wu G, Bondada S, Chen C.
Epstein-Barr virus (EBV)-associated B-cell lymphomas occur more frequently in immunodeficient states such as organ transplantation and HIV infection.
We have previously reported that B cell immortalization (An immortalised cell line is a population of cells from a multicellular organism which would normally not proliferate indefinitely but, due to mutation, have evaded normal cellular senescence and instead can keep undergoing division via tumour cells) with EBV was promoted by cyclosporin A (CyA) and that curcumin (Cur), a natural phenol with known antioxidant and antitumour properties, blocked EBV-induced B cell immortalization.
In the following experiments we show that Cur inhibits the proliferation of EBV-transformed lymphoblastoid cell lines (LCL) via enhanced apoptosis.
LCL were generated by infecting freshly isolated human B cells with EBV (B95-8) for 12 h and coculturing with predetermined optimal concentrations of CyA (500 ng/ml) for 4 weeks. LCL were then either frozen for future use or propagated for immediate experiments. These cells were then plated in 96-well plates with 20 microM Cur or 0.1% DMSO (vehicle control). The number of immortalized colonies/well, cell count, and (3)H uptake were used as an index of immortalization. To assess apoptosis rate LCL were cultured with 0.1% DMSO or Cur (20 microM) for 0, 18, and 42 h in culture flasks and then stained with MC540 and H33342, as markers for apoptosis, and analyzed by FACS.
A profound inhibition of proliferation was seen in the LCL with 20 microM curcumin compared to 0.1% DMSO control. The colony count reduced from 34.5 +/- 3.4 to 0/well (P = 0.005), cell number reduced from 101,250 +/- 12,093 to 3750 +/- 1500/well (P = 0.002), and (3)H uptake reduced from 40,889 +/- 3669 to 70 +/- 5.2/well (P = 0.001). The apoptosis rate of LCL in the DMSO control at 24.07 and 16.87% increased significantly with 20 microM Cur to 76.4 and 95.1% at 18 and 42 h, respectively (P = 0.02).
Curcumin is a potent inhibitor of EBV-transformed lymphoblastoid cell lines (LCL). This effect appears to be mediated through enhanced apoptosis. A further investigation of this effect may be useful in prevention and therapy of B-cell lymphoma in immunodeficient patients.
5. Int Immunopharmacol.2018 Jan;54:177-187. doi: 10.1016/j.intimp.2017.11.009. Epub 2017 Nov 15.
Inhibition of curcumin on influenza A virus infection and influenzal pneumonia via oxidative stress, TLR2/4, p38/JNK MAPK and NF-κB pathways.
Dai J1, Gu L2, Su Y2, Wang Q2, Zhao Y2, Chen X2, Deng H2, Li W3, Wang G2, Li K2.
Oxidative stress, Nrf2-HO-1 and TLR-MAPK/NF-κB signaling pathways have been proved to be involved in influenza A virus (IAV) replication and influenzal pneumonia.
In the previous studies, we have performed several high-throughput drug screenings based on the TLR pathways.
In the present study, through plaque inhibition test, luciferase reporter assay, TCID50, qRT-PCR, western blotting, ELISA and siRNA assays, we investigated the effect and mechanism of action of curcumin against IAV infection in vitro and in vivo.
The results showed that curcumin could directly inactivate IAV, blocked IAV adsorption and inhibited IAV proliferation.
As for the underlying mechanisms, we found that curcumin could significantly inhibit IAV-induced oxidative stress, increased Nrf2, HO-1, NQO1, GSTA3 and IFN-β production, and suppressed IAV-induced activation of TLR2/4/7, Akt, p38/JNK MAPK and NF-κB pathways.
Suppression of Nrf2 via siRNA significantly abolished the stimulatory effect of curcumin on HO-1, NQO1, GSTA3 and IFN-β production and meanwhile blocked the inhibitory effect of curcumin on IAV M2 production.
Oxidant H2O2 and TLR2/4, p38/JNK and NF-κB agonists could significantly antagonize the anti-IAV activity of curcumin in vitro.
Additionally, curcumin significantly increased the survival rate of mice, reduced lung index, inflammatory cytokines and lung IAV titer, and finally improved pulmonary histopathological changes after IAV infection.
In conclusion, curcumin can directly inactivate IAV, inhibits IAV adsorption and replication; and its inhibition on IAV replication may be via activating Nrf2 signal and inhibiting IAV-induced activation of TLR2/4, p38/JNK MAPK and NF-κB pathways.
6. Front Microbiol. 2019 May 3;10:912. doi: 10.3389/fmicb.2019.00912. eCollection 2019.
Anti-infective Properties of the Golden Spice Curcumin.
Praditya D1,2,3, Kirchhoff L4, Brüning J1, Rachmawati H5,6, Steinmann J4,7, Steinmann E1.
The search for novel anti-infectives is one of the most important challenges in natural product research, as diseases caused by bacteria, viruses, and fungi are influencing the human society all over the world.
Natural compounds are a continuing source of novel anti-infectives.
Accordingly, curcumin, has been used for centuries in Asian traditional medicine to treat various disorders. Numerous studies have shown that curcumin possesses a wide spectrum of biological and pharmacological properties, acting, for example, as anti-inflammatory, anti-angiogenic and anti-neoplastic, while no toxicity is associated with the compound.
Recently, curcumin's antiviral and antibacterial activity was investigated, and it was shown to act against various important human pathogens like the influenza virus, hepatitis C virus, HIV and strains of Staphylococcus, Streptococcus, and Pseudomonas.
Despite the potency, curcumin has not yet been approved as a therapeutic antiviral agent.
This review summarizes the current knowledge and future perspectives of the antiviral, antibacterial, and antifungal effects of curcumin.
7. PLoS One. 2013 May 1;8(5):e62482. doi: 10.1371/journal.pone.0062482. Print 2013.
Inhibition of enveloped viruses infectivity by curcumin.
Chen TY1, Chen DY, Wen HW, Ou JL, Chiou SS, Chen JM, Wong ML, Hsu WL.
Curcumin, a natural compound and ingredient in curry, has antiinflammatory, antioxidant, and anticarcinogenic properties.
Previously, we reported that curcumin abrogated influenza virus infectivity by inhibiting hemagglutination (HA) activity.
This study demonstrates a novel mechanism by which curcumin inhibits the infectivity of enveloped viruses. In all analyzed enveloped viruses, including the influenza virus, curcumin inhibited plaque formation. In contrast, the nonenveloped enterovirus 71 remained unaffected by curcumin treatment.
We evaluated the effects of curcumin on the membrane structure using fluorescent dye (sulforhodamine B; SRB)-containing liposomes that mimic the viral envelope.
Curcumin treatment induced the leakage of SRB from these liposomes and the addition of the influenza virus reduced the leakage, indicating that curcumin disrupts the integrity of the membranes of viral envelopes and of liposomes.
When testing liposomes of various diameters, we detected higher levels of SRB leakage from the smaller-sized liposomes than from the larger liposomes.
Interestingly, the curcumin concentration required to reduce plaque formation was lower for the influenza virus (approximately 100 nm in diameter) than for the pseudorabies virus (approximately 180 nm) and the vaccinia virus (roughly 335 × 200 × 200 nm).
These data provide insights on the molecular antiviral mechanisms of curcumin and its potential use as an antiviral agent for enveloped viruses.
FEBS Lett. 2010 Feb 19;584(4):707-12. doi: 10.1016/j.febslet.2009.12.019. Epub 2009 Dec 17.
8. Curcumin inhibits hepatitis C virus replication via suppressing the Akt-SREBP-1 pathway.
Kim K1, Kim KH, Kim HY, Cho HK, Sakamoto N, Cheong J.
A polyphenolic compound from the curry spice turmeric, curcumin, is known to show anti-viral activity against the influenza virus, adenovirus, coxsackievirus, and the human immunodeficiency virus.
However, it remains to be determined whether curcumin can inhibit the replication of hepatitis C virus (HCV).
In this study, we showed that curcumin decreases HCV gene expression via suppression of the Akt-SREBP-1 activation, not by NF-kappaB pathway.
The combination of curcumin and IFNalpha exerted profound inhibitory effects on HCV replication.
Collectively, our results indicate that curcumin can suppress HCV replication in vitro and may be potentially useful as novel anti-HCV reagents.