Propertles Acute Respiratory Syndrome Coronavirus-2 SARS-CoV-2 represents an emergent global propsrties which propertiees straining Quercetin and anti-viral properties healthcare capacity. As of May 27th, the ajti-viral caused by SARS-CoV-2 COVID anti-ciral resulted in more thanQhercetin worldwide, withdeaths pro;erties the US alone.
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Safe, cheap interventions which have a sound biological rationale Qiercetin be prioritized for experimental use in the current Quercetin and anti-viral properties of a lroperties health pandemic. We present the current Quercwtin for the use of vitamin C and quercetin both priperties prophylaxis in high-risk populations and for the treatment of COVID patients as an adjunct to promising pharmacological agents such as Remdesivir or convalescent plasma.
It is serendipitous or Immune system support for cancer prevention indicative of hard work that the Nobel prkperties winner Szent-Gyorgyi discovered both ascorbic acid vitamin C and the anti--viral quercetin at the time labeled vitamin P 1.
Ascorbic Scalability testing tools is an essential vitamin with known Glycogen replenishment for increased exercise capacity properties 2 which is under investigation propegties its beneficial effects during the stress response in Quercetin and anti-viral properties prperties critically ill patients 3.
Vitamin C exerts its antiviral properties by supporting lymphocyte activity, increasing interferon-α production, modulating cytokines, reducing inflammation, improving uQercetin dysfunction, and restoring Superfood supplement for detoxification function 4 — 6.
There are also suggestions nati-viral vitamin C may be directly Quercetij 7. These in vitro effects, as we previously anti-virsl 2constitute a reflection of both Queecetin supra-physiological concentrations of ascorbate and the interaction between vitamin C and metal-containing culture media—both of which are pro-oxidant, Quecretin reactive oxygen species.
Studies suggest that quercetin an may promote antioxidant 9Quercetjn, antiviral 10and immunoprotective effects Quercetin has been studied in various types and models of porperties infection due to its promising antiviral effects Qurcetin inhibiting Ati-viral 12proteases 13reverse transcriptase 14suppressing DNA gyrase, Customized meal plans for athletes binding viral capsid proteins 15 In plants, quercetin propefties produced from the phenylpropanoid pathway anti-vviral is ultimately oroperties from phenylalanine.
It proerties converted to 4-coumaroyl-CoA, via phenylalanine prlperties, to cinnamatehydroxylase and 4-coumaroyl-CoA-ligase. Finally, eriodyctiol is hydroxylated Quercein converted to quercetin Figure anti-vial using flavanol Quercetin and anti-viral properties Figure 1.
Chemical structure of quercetin. Created with Propergies Web with permission Flavonoid compounds, such as Querdetin, were initially studied for their priperties activity in qnd capillary wall andd 19 anti-vviral continue to be investigated andd their effects on DKA and type diabetes tension Dietary supplements differ, but often contain the Quedcetin form of quercetin—quercetin aglycone—under the FDA national znti-viral code numbers Lroperties consumed, quercetin Quervetin predominantly Wound healing surgery into anri-viral large intestine This antioxidant Quercetkn may also be potentiated by ptoperties C 26proeprties will be discussed below.
Anti-vkral biological rationale is secondary to quercetin's free radical Querceton Quercetin and anti-viral properties, alongside propeeties roles identified in in vitro Quercdtin in vivo Quegcetin including: inhibition of platelet aggregation 28inhibition of lipid peroxidation 29and its inhibitory propertes on pro-inflammatory mediators such as Qusrcetin 30 anti-virao phospholipase A2 Relaxation techniques for controlling hypertension, 3-methyl-quercetin, a quercetin metabolite, displays stimulatory effects on nasal epithelial aanti-viral ciliary beat frequency, both Immune system support for cancer prevention vitro anti-viiral in vivowhen anti-vjral either alone or with absorption enhancer HP-β-CD Anti-vral is a tremendous amount of literature supporting the antiviral Querceton of quercetin, in propertiies in vitro and in vivo experiments.
Quercetin inhibits Quercetkn respiratory viruses Anti-biral cultured cells 16anri-viral It inhibits anti-virap cytopathic effects provoked by many serotypes of rhinovirus, echovirus type 7, 11, 12, and 19propeeties A21 and Prolertiesand poliovirus anti-vjral 1 Sabin propegties a QQuercetin inhibitory concentration of 0.
Quercetin prolerties significantly reduces anti-ivral formation by RNA and DNA viruses [Respiratory Syncytial Virus RSV propertiies, Polio type 1, parainfluenza type 3, and Herpes Anti--viral Virus-1 HSV-1 ] displaying anti-infective and anti-replicative properties It inhibits the anc of cytomegalovirus CMV inoculated HeLa cells at a half inhibitory concentration IC50 of 3.
Dengue virus type 2 DENV-2 replication in Vero cells is inhibited by nati-viral at an IC50 of This is attributed to quercetin's ability to either block virus entry or inhibit Quercetiin replication enzymes such as viral polymerases This may suggest that the antiviral effects may be dependent on a minimum inhibitory concentration or from some form of metabolic drug conversion Quercetin treatment also displayed a beneficial effect in immunocompetent mice infected with Mengo virus, where it lessened the severity of organ damage Athletes supplemented with quercetin are protected from stress-induced susceptibility to upper respiratory tract infection 44 —which was not related to immunomodulation 45 Vitamin C is an essential nutrient involved in a diverse array of immune functions; its supplementation has demonstrated beneficial effects in different types of viral infections.
Reduced levels of ascorbate have been found in patients with viral infections 47sepsis 48sepsis-related ARDS 49and other critical illness During infection, vitamin C is necessary for neutrophil killing 51is concentrated within macrophages 52is responsible of T cell maturation 53and promotes phagocytosis and apoptosis of spent neutrophils 4.
It is not surprising, therefore, that viral infections, depending on their severity, are associated with an increased metabolism and reduced Qyercetin ascorbate.
Vitamin C has improved survival in different murine models of lethal infection. Mice incapable of synthetizing vitamin C L -Gulono-gamma-lactone oxidase nulls were infected with influenza; mice not receiving supplemental vitamin C exhibited greater lung pathology scores despite no differences in viral titers Vitamin C administration i.
Vitamin C administered at 1 g BID to patients, reduced the risk OR 0. It is noteworthy that a growing number of case reports of virus-related acute respiratory distress syndromes ARDS indicate successful treatment with intravenous high doses of Vitamin C 62 Co-administration of quercetin quercetin An older, small clinical trial identified the combination of flavonoids and ascorbic acid ratio as beneficial for respiratory infection mg TID Cell entry is a crucial step during viral infection and has been studied as a potential target of antiviral treatments 66 — In an in vitro model of H1N1 and H3N2 influenza infection of MDCK cells, quercetin demonstrated reduced cytopathic effect 48 h post-infection This effect was observed when quercetin was administered during viral entry 0—2 hwas maximal with quercetin pretreatment, and was dependent on quercetin's ability to bind hemagglutinin proteins HA.
Specifically, quercetin bound dose-dependently the HA subunit responsible for membrane fusion during virus entry and virus-mediated hemolysis In vitroquercetin pre-treatment 10 μM inhibited Rhinovirus RV virulence, entry, and replication into BEAS-2B cells via multiple mechanisms: it impeded RV endocytosis though misdirecting EEA1 localization -an early endosomal marker- and inhibiting AKT phosphorylation with subsequent 3-fold viral load reduction at 24 h, lowering negative-strand RNA and modulating interferon IFN and IL-8 expression These results were confirmed in vivowith an estimated lower plasmatic concentration of quercetin nM similarly to other studies 71 — 73 during which quercetin reduced RV-RNA at 1 day post-infection, modulated KC, MIP-2, TNF-a, and MCP-2, decreased virus-induced airway hyper-responsiveness, and modulated IFNs IFN-α and IFN-λ2 In human embryonic kidney cells HEKinoculated with polio, 3-methyl-quercetin disrupted plaque formation while quercetin itself demonstrated these effects when administered together with vitamin C In fact, Vitamin C either D- or L-ascorbate but not dehydroascorbateprevented quercetin spontaneous degradation suggesting necessary co-administration with ascorbate to exert its antiviral effect.
The beneficial effects of 3-methyl-quercetin 10 μM were exerted primarily when the compound was administered 1—2 h post-poliovirus infection in Hela cells, inhibiting viral proteins and RNA synthesis in a dose dependent manner In fact, 3-methyl-quercetin was identified as a molecule able to bind essential proteins required during the transcription from minus-strand RNA into positive polarity RNAs, thus interfering with cytoplasmic viral RNA replication These beneficial effects were ascribed to a complete inhibition of virus replication when the compound was added within 2 h after virus absorption and related to the blockade of the RNA polymerase complex, as demonstrated in vitro Quercetin has been investigated in vitro as an antiviral agent for HIV due to its ability to inhibit crucial enzymes: reverse transcriptase RTintegrase INand protease PR Quercetin significantly reduces HIV viral replication 81 and, when added to peripheral blood mononuclear cells PBMNc infected with HIV and compared to HIV infected controls, quercetin reduced the levels of p24, Long Terminal Repeat LTR gene expression, and viral infectivity together with an inhibition of TNF-α and upregulation of IL Quercetin has also been shown to inhibit non-HIV RT activity in vitroincluding avian myeloblastosis reverse transcriptase AMV-RTRous-associated virus-2 RAVRTand Maloney murine leukemia virus MMLV-RT.
Interestingly, Harakeh et al. Quercetin is a potent HIV protease inhibitor in vitrowith an IC50 of Quercetin treatment inhibits HCV replication This effect is attributed to its ability to modulate Heat Shock Protein expression HSPsthus impeding the crucial binding between heat shock factor and elements HSF-HSE necessary for the stress-induced transcription of stress genes 85 Quercetin reduced HSP70 and HSP40, thereby impeding the formation of Non-Structural protein 5A complexes NS5A-HSP70 and NS5A-HSP40 necessary for HCV genome replication apparatus through the internal ribosome entry site IRES.
Despite unaltered HCV titer, the production of infectious particles was decreased, interestingly more by quercetin treatment than by HSP knockdown, displaying a dose-dependent relationship: at 0.
Quercetin stimulates T-helper cells to produce Th-1 -derived Interferon-γ IFN- γ and downregulates Th2-derived IL-4 when added to cultured blood peripheral mononuclear cells Immunonutrition studies in pgoperties with supplementary polyphenols, including quercetin, showed enhanced NK cell lytic activity, neutrophil chemotaxis, and lymphocyte proliferation 87 Human foreskin fibroblast HFF and endothelial cells EC pretreated with 2-phospho-ascorbate ASC-2P resisted CMV infection; they displayed a reduction in immediate and late antigens and viral yield was inhibited 50—fold in ECs and —1,fold in HFF This effect was not dependent on a sustained ASC-2P presence but was abolished if the ASC2-P was added after the virus infection, indicating an immunomodulatory effect, rather than directly antiviral.
Patients with acute Epstein-Barr infection EBV treated with high doses of intravenous vitamin C 7. Vitamin C administration has been related to enhanced interferon production and was studied for its possible use for the prevention of vaccine failure. Low levels of vitamin C, in fact, have been related to insufficient phosphorylation of signal transducers and activation of transcription STATswhich represent a crucial signaling process of IFNs Specifically, T cells of mice deficient in vitamin C display defects in STAT3 phosphorylation SARS-Coronavirus, described in 99is a single-stranded RNA virus of ~29, nucleotides, which uses ribosome sites to encode two replicase glycoproteins, PP1a and PP1b, that mediate viral replication 99 Once these precursor glycoproteins are synthesized, 3C-like protease 3CLpro plays a critical role in the lytic release of its replicates Quercetin-3β-galactoside binds SARS-Cov 3CL protease and inhibits its proteolytic activity with an IC50 of This inhibitory action on 3CLpro is dependent on the hydroxyl group of quercetin which, as shown through molecular modeling and QA mutation, recognizes Gln as a crucial site on 3CLpro responsible for the binding of quercetin Quercetin was also identified as a compound able to block SARS-Coronavirus entry into Vero E6 cells with a half-effective concentration EC50 of SARS-CoV-2, the virus responsible for the COVID pandemicbelongs to the genus Betacoronavirus and subgenus Sarbecovirus and, due to its similar receptor-binding domain, it is assumed, similarly to SARS-CoV, to infect type II pneumocytes entering via the angiotensin-converting enzyme II receptor SARS-Cov-2 protease 3CL maintains the same Gln site of SARS-Cov 3CLpro, which previously was identified as the binding site Querrcetin the hydroxyl groups of quercetin Queretin its derivates Interestingly, an in vitro study of ascorbic acid treatment on chick-embryo ciliated tracheal organ cells CETO promoted resistance to Coronavirus infection but did not show any effect on orthomyxovirus or paramyxovirus Despite the breadth and depth of anti-viral in vitro and in vivo studies into the immunomodulatory effects of quercetin and vitamin C administration, further studies are absolutely necessary to confirm quercetin inhibitory activities on SARS-Cov-2 virus entry, RNA polymerase, and on other necessary viral life-cycle enzymes.
Orally administered quercetin glycosides are hydroxylated by β-glucosidases in the gut Indeed, four out of five hydroxyl groups of quercetin can be glucuronidated by UDP-glucuronosyltransferase, forming its major metabolites: quercetinglucuronide, 3'-methylquercetinglucuronide, and quercetin-3'-sulfate Rat tissue distribution of orally, long-term administered quercetin 12 weeks shows the highest concentration in the lungs while pigs display the highest concentrations in the liver and kidneys In contrast, short-term administration exhibits no marked distribution, implying that the beneficial effects of quercetin in preventing lung respiratory viral infection could be maximized by long-term administration.
Intravenous administration results in an elimination half-life of 0. Only higher intravenously administered doses up to The safety of quercetin-based oral supplementation during pregnancy and breastfeeding has not been established.
We have previously described the safety profile and dosing strategies of vitamin C According to the data presented above, we propose the following optimal dosing Table 1. Table 1. Proposed multi-drug approach for either the prophylaxis for high risk population, and treatment of mild and severe cases.
However, QQ can be recycled into quercetin by electron donors like NADH or ascorbate, or form together, with glutathione either 6-glutathionyl-quercetin or 8-glutathionyl-quercetin GSQs ,
: Quercetin and anti-viral properties| Top bar navigation | Sun D, Li C, Chen S, Zhang X Emerging role of dendritic cell intervention in the treatment of inflammatory bowel disease. Br J Pharmacol. McClure J et al Silibinin inhibits HIV-1 infection by reducing cellular activation and proliferation. Quercetin enhances the colonic glutathione GSH reservoirs and nuclear factor erythroid 2-related factor 2 Nrf2 , protecting the intestinal porcine epithelial cell line 1 IPEC-1 cells Jia et al. They can cause seasonal outbreaks and, as we are now seeing with COVID, a worldwide pandemic that impacts public health as well as the economy. Ann N Y Acad Sci — Article CAS PubMed Google Scholar Dayem AA, Choi HY, Kim YB, Cho S-G Antiviral effect of methylated flavonol isorhamnetin against influenza. Flavonoid compounds, such as quercetin, were initially studied for their biological activity in affecting capillary wall resistance 19 and continue to be investigated for their effects on vascular tension |
| REVIEW article | Miri ST, Sotoodehnejadnematalahi F, Amiri MM, Pourshafie MR, Rohani M The impact of Lactobacillus and Bifidobacterium probiotic cocktail on modulation of gene expression of gap junctions dysregulated by intestinal pathogens. Inhibition of reverse transcriptases by flavonoids. Antiviral Res 75 3 — Jia H et al Quercetin alleviates oxidative damage by activating nuclear factor erythroid 2-related factor 2 signaling in porcine enterocytes. Download references. The aglycone version of quercetin is highly water insoluble and lipophilic. |
| Antiviral Effects of Quercetin through Zinc Ionophore Activity - GilbertLab | Inhibition of rhinovirus replication at various stages by quercetin. Likewise, quercetin enhances viral clearance via mitochondrial antiviral response [ 10 ]. Typical influenza lesions including interstitial pneumonia and necrotizing bronchiolitis were also noticed. Q3R administration on influenza-infected mice showed moderate inflammation including pulmonary edema and elevated numbers of inflammatory cells and necrosis. Particularly, a dose of 6. Moreover, the result of the CPE 50 assay to determine the viral titer in the mice lung demonstrated the average titer for Q3R-treated mice was approximately lower than that of the placebo group and two times lower than that of the oseltamivir-treated group. Intriguingly, Q3R and oseltamivir treatment given for influenza uninfected mice displayed similar histopathological results to placebo-controlled mice [ 11 ]. The influenza virus envelope protein hemagglutinin has been targeted to block the viral entry by pretreatment and co-treatment with quercetin [ 12 ]. It revealed that quercetin generated an obvious inhibitory action against H3N2 and H1N1 virus strain infections in a dose-dependent manner. The inhibitory effect was pronounced when the virus was preincubated with quercetin or when quercetin was added to the virus-infected cells MDCK and A cells. Based on the time of additional assay, quercetin effectively acts during the viral entry stage, while inhibitory effects during or after infection were less clear. Furthermore, the results confirm that quercetin generated a strong binding affinity to the HA2 subunit of influenza A virus Fig. Illustration of influenza virus life cycle and the pathways modulated by quercetin. Influenza virus utilizes hemagglutinin HA receptor for binding and entry. Moreover, membrane-2 M2 ion channel promotes fusion and uncoating, and neuraminidase NA facilitates the progeny virus release. Collectively, quercetin interferes at different steps including viral binding, uncoating, mRNA synthesis, negative-strand synthesis, assembly, and release [ 12 ]. There has been some evidence during acute influenza virus infection that oxidative stress plays a crucial role in the living cells affected [ 13 ]. This process eventually promotes lung injury, apoptosis, inflammation, or allergy and further alters cellular metabolism, particularly mitochondrial function resulting in mitochondrial ROS production [ 13 , 14 ]. However, quercetin supplementation failed to increase the vitamin E level significantly in both normal and infected-H3N2 mice models. The study concluded that quercetin proved to raise the antioxidant concentration in the lung and bring them nearly to normal levels. These findings consistently supported that quercetin demonstrated the ability to block ROS production by neutrophils, particularly by blocking protein kinase C PKC , an enzyme that activates NADPH oxidase and respiratory burst [ 15 ]. A previous in vitro study by Wan et al. showed that quercetin has the ability to reduce the mRNA and protein overexpression of cyclin-dependent kinase-4 CDK4 in A lung epithelial tumor cells infected with H1N1 [ 16 ]. The expression of CDK4 mRNA and protein in H1N1-infected cells treated with quercetin and ribavirin was significantly lower than in untreated infected cells. Albeit the direct antiviral action of quercetin on H1N1 was not as strong as ribavirin, the result showed quercetin was less toxic and able to inhibit CDK4 mRNA and protein overexpression in H1N1-infected A cells. These findings are presumably due to the ability of quercetin to induce DNA repair, thus promoting host cell proliferation [ 16 ]. Another study by Gansukh et al. Likewise, virus-induced ROS and autophagy formation were also evaluated. Human respiratory syncytial virus hRSV , a member of the family Pneumoviridae, is an important pathogen in the development of acute lower respiratory infection ALRI and a major cause of hospitalization in the pediatric population worldwide. To date, the existing treatment and management of hRSV infections like the use of palivizumab and ribavirin encounter challenges. For instance, difficulty in administration, the generation of drug escape mutants, substantial side effects, long-term administration, low efficacy against the virus, and expensive cost are entailed in prophylaxis. Hence, some researchers have been done to discover alternative compounds or design new strategies against hRSV to suppress its spread and halt the infection [ 18 ]. Quercetin is a bioactive flavonoid that confers several biological effects, including anti-hRSV [ 19 ]. Notwithstanding, the issue still exists pertaining to low solubility and low stability of quercetin in the lipophilic media of a membrane owing to the presence of hydroxyl groups [ 20 ]. A previous study done by Lopes et al. used quercetin as a parent compound Q0 and acetylation of quercetin; quercetin pentaacetate Q1 was tested on Hep-2 cells infected with hRSV to evaluate its capability in halting the viral entry and replication [ 21 ]. Initially, cytotoxicity of Q0 and Q1 was done in incubated Hep-2 cells in the selected range of concentration 0. The results revealed that the Q1 had lower cytotoxicity than the Q0. As compared to Q0, Q1 showed relevant cell protection 2. Likewise, in a dose-dependent manner, the infected cells treated with Q1 revealed a reduction of syncytia formation, no cell detachment in post-treatment at the lowest MOI, and a great reduction of syncytia formation in the virucidal assay at MOI 0. Concerning cytotoxicity, it has been shown that Q1 is more hydrophobic than Q0. Hence, Q1 would penetrate cells by which it is protected by degradation of extracellular space [ 22 ]. To further understand, in silico analysis was done in the same study to prove that the compound may interact with the F-protein of hRSV [ 21 ]. Similar to G, the F-protein has been established to interact with cellular heparan sulfate or immobilized heparin, facilitating attachment to and infection of immortalized cells [ 18 ]. The study verified the effect of Q1 on the stability of the hRSV-F modeled hRSVmF -Q1 complex and used the hRSVmF-JNJ as reference control. Q0 demonstrated an escaping trend from the hRSVmF central cavity, which did not happen with the reference ligand. Intriguingly, Q1 exhibited a closer interaction with the cavity when compared to Q0 and towards the end of the trajectory demonstrated a similar pattern to the reference ligand. There were no hydrogen bonds observed between Q1 and hRSVmF cavity residues, showing the occurrence of hydrophobic interactions. Albeit Q1 exhibited lower electrostatic contributions and did not exert hydrogen bonds with hRSVmF cavity residues, the interaction energy of Q1 is higher than that observed for Q0, indicating the structural differences between the two molecules. The chemical modification from Q0 to Q1 implies the replacement of the hydroxyl group for acetyl, hence resulting in greater affinity for the cavity hRSVmF [ 21 ]. The hRSV cycle entails adsorption, internalization, transcription, translation, assembling, and budding. Previous studies revealed that the hRSV infection cycle is complete in about 24—48 h postinfection hpi [ 23 ]. According to the same study, the effect of Q1 in the hRSV cycle was tested in adsorption, internalization, and time addition protocols with MOI 0. The result showed that Q1 exhibits great protection on adsorption assay in all tested concentrations 1. Notwithstanding, in internalization protocol, Q1 did not exhibit any effect on hRSV infection. Moreover, Q1 at 6 μM only exhibited significant protection in time addition protocol in 0 and 36 hpi [ 21 ]. Another important target protein possessed by hRSV is the M protein. It is an essential anti-termination factor for the transcription process that averts the premature dissociation of the polymerase complex. Hence, it becomes a potential target for the development of viral replication inhibitors [ 24 ]. A study done by Guimaraes et al. evaluated the interaction of Q1 and tetraacetylated Q2 quercetin derivatives with the M tetramer. The acetylation was done to generate a stronger bioactive compound against the oxidation process. To further understand the formed interaction, molecular docking was done, and it demonstrated that the possible binding site takes place between the globular domain α-helix 6 from one monomer with the zinc finger domain from other monomers of the tetramer. Providing these results, acetylated quercetin renders its potential as an hRSV inhibitor since it was able to generate binding sites in the viral RNA-binding domain. Human metapneumovirus hMPV is known as the major cause of lower respiratory tract infections, for instance, bronchiolitis and pneumonia in pediatrics, elderly, and immunocompromised individuals. Notwithstanding, the economic impact on the pediatric population is similar to that of the influenza virus [ 25 ]. To date, hMPV infection of airway epithelial cells stimulates pro-inflammatory gene expression via activation of transcription factor nuclear factor kappa B NF-κB p65 subunit and interferon regulatory factor IRF Likewise, both in vitro and in vivo, it stimulates oxidative stress by progressively deteriorating gene expression and protein levels of antioxidant enzymes like superoxide dismutase-3, catalase, and glutathione S-transferase. The nuclear translocation of the transcription factor Nrf2 was also known to be reduced in hMPV infection [ 26 ]. An in vitro study was done using A cells alveolar type 2 cancerous cell line that were infected with hMPV at an MOI of 1 [ 25 ]. Following h postinfection, there was evidence of an increased level of 8-isoprostane oxidative stress damage marker , CXCL8 IL-8 , CCL5 RANTES , IL-1α, IL-6, TNF-α, CXCL10 IP , and CCL4 MIP-1β. Treatment with both resveratrol 10—50 μM and quercetin 1—10 μM in a dose-dependent manner was significantly able to suppress the expression of these cytokines and chemokines [ 25 ]. Moreover, treatment with resveratrol and quercetin given h post-infection was associated with a much lower viral titer, as compared to control untreated but infected by hMPV. In the resveratrol group, the viral titer declined from almost a million per mL to 50,, and in quercetin group, the viral titer declined to a little above , [ 25 ]. This study also investigated whether resveratrol and quercetin could suppress the activation of pro-inflammatory cytokines NF-κB and IRF-3 activation. The result demonstrated that hMPV infection caused significant p65 subunit and IRF-3 nuclear translocation. Likewise, treatment with resveratrol and quercetin significantly reduced these actions, thus suppressing the subsequent release of pro-inflammatory cytokines and chemokines [ 25 ]. All these studies explained how quercetin and its derivatives demonstrate a wide spectrum of antiviral activities on respiratory illnesses induced by various viral infections. Albeit many in vitro studies exist, clinical studies using human subjects are still lacking. It would be of extreme importance to focus on the utilization of quercetin for prophylaxis or preventive purposes, as well as in combination with other medications. Hence, it could enhance or promote synergistic interactions between the substances and reduce the adverse effects and related toxicity and increase the overall safety and efficacy. Ryan ET, Hill DR, Solomon T, Aronson NE, Endy TP 32 - Viral infections with cutaneous lesions. Elsevier, London, pp — Chapter Google Scholar. Burk M, El-Kersh K, Saad M, Wiemken T, Ramirez J, Cavallazzi R Viral infection in community-acquired pneumonia: a systematic review and meta-analysis. Eur Respir Rev. Article PubMed PubMed Central Google Scholar. Shi T, McLean K, Campbell H, Nair H Aetiological role of common respiratory viruses in acute lower respiratory infections in children under five years: a systematic review and meta-analysis. J Glob Health. Article Google Scholar. Rizky WC, Jihwaprani MC, Kindi AA, Ansori ANM, Mushtaq M The pharmacological mechanism of quercetin as adjuvant therapy of COVID Life Res. Anand David AV, Arulmoli R, Parasuraman S Overviews of biological importance of quercetin: a bioactive flavonoid. Pharmacogn Rev. Choirur Rizky W, Candragupta Jihwaprani M, Mushtaq M Protective mechanisms of quercetin in various lung-induced injuries. SCIREA J Clin Med. Anwar E, Soliman M, Darwish S et al Mechanistic similarity of immuno-modulatory and anti-viral effects of chloroquine and quercetin the naturally occurring flavonoid. Clin Immunol Res. Google Scholar. El-Saber Batiha G, Magdy Beshbishy A, Ikram M et al The pharmacological activity, biochemical properties, and pharmacokinetics of the major natural polyphenolic flavonoid: quercetin. Foods Article CAS Google Scholar. Farazuddin M, Mishra R, Jing Y, Srivastava V, Comstock AT, Sajjan US Quercetin prevents rhinovirus-induced progression of lung disease in mice with COPD phenotype. PLoS One. Article CAS PubMed PubMed Central Google Scholar. Ganesan S, Faris AN, Comstock AT et al Quercetin inhibits rhinovirus replication in vitro and in vivo. Antiviral Res. Choi HJ, Song JH, Kwon DH Quercetin 3-rhamnoside exerts antiinfluenza A virus activity in mice. Phyther Res. Kumar P, Khanna M, Srivastava V, Tyagi YK, Raj HG, Ravi K Effect of quercetin supplementation on lung antioxidants after experimental influenza virus infection. Exp Lung Res. Article CAS PubMed Google Scholar. Chen K-K, Minakuchi M, Wuputra K et al Redox control in the pathophysiology of influenza virus infection. BMC Microbiol. To EE, Erlich JR, Liong F et al Mitochondrial reactive oxygen species contribute to pathological inflammation during influenza a virus infection in mice. Antioxid Redox Signal. Ciz M, Denev P, Kratchanova M, Vasicek O, Ambrozova G, Lojek A Flavonoids inhibit the respiratory burst of neutrophils in mammals. Oxid Med Cell Longev. In a tissue culture study, the administration of quercetin to cells infected with hepatitis C resulted in a marked reduction of viral load as a result of HSP synthesis inhibition [6]. This study concluded that HSP synthesis inhibition may be an attractive therapeutic avenue in reducing viral replication, especially in people who have HCV genotype 1 which does not respond well to the standard hepatitis C antiviral treatment protocol of interferon-gamma and ribavirin. The administration of quercetin to infected cells was successful at reducing viral load and was therefore determined to be a potentially effective adjunct in the treatment of hepatitis C with low associated toxicity. Quercetin also fortifies the immune response by promoting early interferon production, modulating interleukins and promoting T cell maturation and phagocytic activity. Most in vitro research suggests that quercetin possesses anti-inflammatory properties and immunological improvement through its ability to modulate cell-signaling pathways that activate and inhibit various targets within the innate and adaptive immune system. Quercetin exerts benefits on cardiovascular protection, reduces hypertension and improves type 2 diabetes through various mechanisms leading to potential improvement in comorbid states associated with a poor prognosis for COVID [ 7 , 8 , 9 ]. Quercetin is found in many plant-based foods including fruits, vegetables, tea, coffee, nuts, seeds and grains. Foods with the highest concentration of quercetin are apples, citrus fruits, capers, onions, shallots, grapes, tomatoes, berries and brassica vegetables. Beverages that have a high concentration of quercetin include red wine and green tea which are also of noted benefit for their respective concentrations of resveratrol and epigallocatechin gallate EGCG which are 2 additional flavonoids recommended for immune and antioxidant support. The higher our consumption of color-rich, plant-based foods, the better chance we have of getting a variety of flavonoids, including quercetin. The Mediterranean diet is often discussed because of various health benefits due to its high concentration of vegetables rich in flavonoids and nutrients that work in a synergistic fashion to optimize individual health. Pure quercetin exists in the form of an aglycone which lacks the attached sugar molecule. The aglycone version of quercetin is highly water insoluble and lipophilic. Quercetin glycoside has a sugar side chain which makes it more water soluble and increases its absorption. Differences in quercetin-conjugated glycosides affect its bioavailability. Quercetin glucoside, or isoquercetin, tends to have the best absorption a s it is more bioavailable due to the highly efficient hydrolysis and absorption of glucoside chains within the enterocytes of the intestinal wall. Overall, quercetin can have variable bioavailability which is why adequate consumption of dietary sources and adequate supplementation early as a preventive measure provides the opportunity for quercetin to accumulate in cells and more readily exert its effects upon exposure to a virus. The majority of studies demonstrate that pretreatment rather than posttreatment of cells produces the best protection against viral replication and cell death. Due to its lipophilic nature, the absorption of quercetin from foods and supplements is facilitated when consumed with dietary fats [10]. More recent formulations of quercetin involve the use of a lecithin base to create a quercetin phytosome. This formulation increases absorption of quercetin by 20 times compared to that of a standard dose of quercetin that is not encased in a phospholipid. Dosage of quercetin ranges between mg for prevention and mg for treatment of viral infections. There are currently a few studies listed in ClinicalTrials. gov on the use of quercetin, either alone or in combination with other nutrients for the prevention and treatment of SARS-CoV-2 in high risk populations with dosing ranging from mg to mg per day. Quercetin, zinc, and vitamin C supplements are inexpensive, well-tolerated and recommended for general immune support and reduction of viral illness. These nutrients also work together in a synergistic capacity to enhance their individual actions. All have a good safety profile if used at recommended dosages and can be used for long periods of time without any negative effects. Viral replication occurs early in the disease process of COVID and may determine the severity of the inflammatory phase which occurs later in the disease process and has the potential to advance to a cytokine storm, especially in those with comorbid conditions and nutrient deficiencies. Early interventions to reduce viral penetration and replication and control the inflammatory response may be key to better outcomes with COVID Using these nutrients preventatively as well as incorporating food sources provides the best results as it allows time for quercetin to equilibrate to optimal tissue levels. If we are adequately fortified with quercetin and other nutritional antivirals prior to viral exposure, the immune system will be better prepared to respond swiftly and effectively to help reduce the duration and severity of the viral infection and inflammatory response cytokine storm. In Part 2 of this 3-part series we will examine the role for zinc in supporting the immune response. Call us at Become a Provider Find a Provider Order Kits. The ZRT Laboratory Blog The ZRT Blog is an extensive resource for patients and health care providers searching for health and hormone testing information. Twitter Facebook LinkedIn Instagram. Naturopathic Therapy for Prevention and Support of Viral Illness: Part 1 — Quercetin Tracy Tranchitella, ND Friday, December 04, When and how to intervene with naturopathic therapies Daily consumption of specific nutrients and natural compounds through diet and supplementation provides the greatest benefit for prevention and treatment of viral infections. Quercetin exerts benefits on cardiovascular protection, reduces hypertension and improves type 2 diabetes through various mechanisms leading to potential improvement in comorbid states associated with a poor prognosis for COVID Categories: Covid Please enable JavaScript to view the comments powered by Disqus. comments powered by Disqus. Posts by Author Alyssa Burns Hill, PhD, MSc, FRSPH, MIHPE Amen Clinics Candace Burch Christina Cowger, MA, LMFT Dr. Alison McAllister Dr. Allison Smith Dr. Beth Baldwin Dr. David Zava Dr. Elise Schroeder Dr. Felice Gersh Dr. James Greenblatt Dr. Julie Verfurth Dr. |
| Background | Previous studies have shown that the quercetin is also a TXNIP inhibitor. In addition, the quercetin inhibits the ASC oligomerization, which is essential for the NLRP3 inflammasome activation. Copy to clipboard. The acetylation was done to generate a stronger bioactive compound against the oxidation process. Leibovitz B, Siegel BV. |
| Protective mechanism of quercetin and its derivatives in viral-induced respiratory illnesses | Common foods include blueberries, red onions, broccoli, cauliflower, kale, and many nuts. Quercetin has been shown to offer strong antioxidant and anti-inflammatory benefits, along with anti-hypertensive, anticoagulant, and anti-hyperglycemic properties. A previous study demonstrated that quercetin could help protect patients from dying from severe complications associated with the H1N1 influenza A virus; however, the exact mechanism was unknown. In a study published in Viruses, researchers investigated the effects of quercetin as an anti-viral agent. The impact of viruses vary. They can cause seasonal outbreaks and, as we are now seeing with COVID, a worldwide pandemic that impacts public health as well as the economy. There have been several other highly impactful infections such as the H1N1 swine flu, H5N1 avian influenza, and H7N9 influenza virus, which can lead to acute respiratory distress syndrome, pulmonary compromise, and death. Due to the lack of drugs to treat t hese infections, natural compounds are a major area of anti-viral research discovery. The life cycle of the influenza virus consists of viral attachment, entry, replication, and release. This study demonstrated that quercetin can inhibit the entry of an influenza virus in the early stage of infection, measuring the inhibition in a cell infection model. This is the initial step of the viral replication cycle. In addition, the research team noted that this inhibitory effect was increased when the virus was pre-incubated with quercetin. It is also important to note that, being an antioxidant and having anti-inflammatory properties, quercetin helps reduce the expression of pro-inflammatory cytokines and lung inflammation in mice. As a result, quercetin may be an inexpensive yet effective natural polyphenol, providing support during influenza infections. It may also be considered in combination with other therapeutics and drugs, which could support their anti-viral effect while helping reduce drug dosage and side effects. Dosage range for quercetin supplementation is often between mg to mg. Nevertheless, Quercetin is currently in the recruiting phase of a clinical trial to establish its efficacy for the prophylaxis and treatment of COVID Ionophores are lipid-soluble and are typically biosynthesized by microorganisms. Their mechanism of transfer involves reversibly binding to ions and releasing them on one or the other side of a cell membrane. These can be proteins or a wide range of other lipid-soluble molecules with properties that are capable of reversibly binding to an ion. These ion channels can thus be regulated and controlled. In industry, ionophores are especially of interest in the development of antibiotics and other pharmaceuticals. For example, antibiotics may have difficulty entering into cells if they are hydrophobic. Thus, pharmaceutical development often needs to make use of endogenous ionophores to facilitate the antibiotic entering through the cell membrane. Ionophores are not typically antibiotics in and of themselves. However, they do facilitate the movement of electrically charged molecules through cell membranes — and these charged molecules may have antibiotic properties. However, some antibiotics — for example the macrolide group — do work as ionophores. High concentrations of sodium, potassium, as well as zinc, have been shown to have potent antibiotic effects. This is especially interesting when looking at ionophores for zinc — like Quercetin and even some quinolone-based antimalarial treatments like Chloroquine. Zinc has long been known for its potential antiviral effects. For example, over-the-counter remedies containing zinc with vitamin C have been shown to reduce the duration and symptoms of the common cold. Zinc is an essential trace element that supports growth and development in children, and a healthy immune system in adults. Nevertheless, non-clinical zinc deficiency remains very common around the world. There are numerous mechanisms of action through which zinc acts against viruses in the human body. These include but are not limited to :. As you can see, zinc has a great many ways in which it helps to protect the body against viral infections. In response to the outbreak of SARS in and SARS-CoV-2 in , researchers doubled down on efforts to understand the mechanisms and potentials of naturally-occurring zinc ionophores like Quercetin and other plant polyphenols. This was especially interesting since zinc has previously been shown to inhibit coronavirus and Arterivirus RNA polymerase activity in vitro. 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