Your Guide to the most Powerful Natural Antivirals available

As someone who has spent years immersed in the world of natural healing, I believe it’s never been more crucial to understand and utilise the power of natural antivirals. In today’s world, where viral threats are no longer distant possibilities but everyday realities, supporting the body’s ability to resist, recover from, and even outsmart viral infections has become essential. The days of relying solely on pharmaceuticals to “step in when needed” are fading fast, replaced by a growing awareness that our immune resilience must be cultivated, not outsourced. From long-established viruses like Herpes and Epstein-Barr to more recent challenges like Long-COVID, we’re seeing a rise in chronic viral burdens that quietly drain our energy, disturb our mental clarity, and weaken our health at its very roots. And yet, nature has always offered powerful allies, compounds that not only inhibit viral replication but also strengthen the body at a foundational level. This Guide is really to the point because it has to be, it has got to show you how powerful these antivirals really are to give you confidence in using them, I will at the end touch on other supportive measures.

Now, let me say something that might surprise a few of you... I don’t actually believe that viruses are fake. I know, shocking. In a world where I’ve entertained everything from free energy devices buried under the Vatican to fluoride being a mind-control agent (which, let’s be honest, it is), this is one conspiracy I just can’t get behind. I’ve seen the effects of chronic viral load first-hand, in people battling Herpes, EBV, even lingering symptoms post-COVID and it’s very real. The viral world exists, and it’s clever, adaptive, and absolutely something we need to take seriously. So yes, viruses are real, and no, they’re not just “exosomes with bad PR.” For once, I’m siding with the scientists on this one… well, the ones who haven’t sold their soul to Big Pharma. But don't worry you know I'm not vaccinated and I am also sure covid was made in a lab, the release... who knows exactly. But it did damage people, and in this article, I’ll be sharing what I consider to be the most potent, well-researched, and time-tested natural antivirals available today substances that belong in every holistic health toolkit. Let’s explore how we can move beyond symptom suppression and into true biological sovereignty. I rank these moves as absolutely essential in health/life... Immune System Function, Body Free of Viruses, Body Free of Inflammation, Mental Wellbeing in balance and peace. Those things, anyway I digress, this Guide is purely on what the best Antivirals are, it's not a protocol for a specific virus it's what antivirals to use, I'll cover only the very best rather than endless effective ones, so it doesn't mean one not listed doesn't work and work really well, it's just I think these are the most consistently effective.

Methylene Blue (MB)

Methylene Blue (MB), a phenothiazine dye first synthesised in the late 19th century, has re-emerged in recent years as a compound of significant interest in antiviral research. While its historical use spans various therapeutic applications, the antiviral effects of Methylene Blue are increasingly being scrutinised and appreciated in the context of persistent and emerging viral threats. Notably, these effects are not anecdotal nor speculative; they are underpinned by a growing body of peer-reviewed research that demonstrates potent activity against a broad spectrum of viruses, including both enveloped and non-enveloped pathogens. I'm going to go deep on this because this is so important, I'll share evidence for its use against specific viruses too. The antiviral properties of Methylene Blue are primarily attributed to its redox activity and photodynamic potential. In its oxidised form, MB can generate reactive oxygen species (ROS), particularly singlet oxygen, which are capable of inactivating viral particles through oxidative damage to viral nucleic acids and proteins. This mechanism is especially pronounced when MB is used in conjunction with light exposure (photodynamic therapy), but crucially, studies have shown that MB retains antiviral effects even in the absence of light. One of the most significant antiviral pathways involves the disruption of viral replication through intercalation into viral RNA or DNA, impairing transcription and genome stability. This has been observed in vitro across several RNA viruses, including Flaviviruses, Coronaviruses, and Retroviruses. MB also demonstrates the ability to disrupt viral envelope integrity, rendering viruses non-infectious by compromising the structural components essential for host cell entry.

SARS-CoV-2 (COVID-19): During the COVID-19 pandemic, Methylene Blue garnered attention for its in vitro efficacy against SARS-CoV-2. A 2021 study published in Biochemical and Biophysical Research Communications demonstrated that MB significantly reduced viral RNA levels in infected Vero E6 cells, even at low micromolar concentrations and in the absence of UV light. The authors concluded that MB acts by blocking the interaction between the virus and host cells, as well as interfering with post-entry replication stages. In addition, a 2020 paper in Photodiagnosis and Photodynamic Therapy highlighted MB’s photodynamic activity as a powerful adjunct to viral inactivation in respiratory secretions, suggesting a role in reducing transmission via mucosal surfaces.

Dengue Virus and Zika Virus: Research has also demonstrated MB’s efficacy against Flaviviruses such as Dengue and Zika. A study in Antiviral Research (2018) found that MB inhibited Zika virus replication in human neuroblastoma cells with notable efficiency. Mechanistically, the inhibition was linked to ROS generation and interference with the viral envelope proteins critical for membrane fusion and entry.

HIV: MB has been studied since the 1990s for its anti-HIV properties, particularly in the context of blood product sterilisation. One prominent mode of action involves photodynamic inactivation, which has been used to treat plasma and prevent HIV transmission. More recently, in vitro studies have shown that MB can interfere with reverse transcriptase activity and reduce viral load independently of light exposure, offering potential as a systemic antiviral under specific dosing regimens.

Herpes Simplex Virus (HSV): Methylene Blue has also demonstrated promising results against Herpesviridae. A study published in Journal of Antimicrobial Chemotherapy reported that MB inhibited HSV-1 and HSV-2 replication in epithelial cell lines. Inhibition occurred via oxidative damage to the viral genome and suppression of immediate early gene expression—critical steps in the HSV lifecycle

How to use Methylene Blue

This is my suggestion for antiviral use only, must be the 1% MB solution. 1% solution = 10 mg/mL, so... 1 drop = 0.5 mg, therefore 1ml (20 drops) = 10mg. Perhaps start with 1 drop (0.5 mg) in water once daily, and observe for 2–3 days before increasing.

0.5 - 4mg per dose, 1-2 x daily
This equals roughly 1-4 drops, depending on body weight and sensitivity.

Dosing Guideline by Weight (rough guide)

Body WeightStarting DoseMax Dose (short-term)
< 60 kg (132 lbs) 0.5–1 mg~2 mg
60–80 kg (132–176) 1–2 mg~3 mg
> 80 kg (176+ lbs) 2–3 mg~4 mg

Lugols Iodine

The use of Iodine in clinical settings has long been associated with its antimicrobial properties, particularly in wound care and disinfection. However, the antiviral efficacy of Lugol’s Iodine—a solution of elemental iodine (I₂) and potassium iodide (KI) in water—extends far beyond topical antisepsis. Increasingly, Lugol’s Iodine is being examined for its systemic and mucosal antiviral effects, with a growing body of evidence supporting its role in both direct viral inactivation and enhanced mucosal immunity. In the face of persistent and emerging viral challenges, iodine's ability to neutralise pathogens at the site of entry and within host tissues deserves serious attention. The antiviral properties of iodine are primarily virucidal. Iodine acts as a halogen oxidant, disrupting viral structure through the oxidation of amino acid residues in viral proteins—particularly those rich in tyrosine and cysteine. This process leads to the denaturation of essential viral enzymes and capsid or envelope proteins, rendering the virus non-infectious. For enveloped viruses, iodine appears to be especially potent due to its action on the lipid bilayer and glycoprotein complexes involved in host-cell entry. Unlike many antiviral compounds that require metabolic activation or immune mediation, iodine’s effects are immediate and non-specific, allowing it to inactivate a wide range of viruses on contact. Importantly, Lugol’s Iodine also contributes to endogenous antiviral defence mechanisms. Iodide, when present in mucosal secretions (such as in the respiratory tract), can be oxidised by the enzyme lactoperoxidase to produce hypoiodous acid (HOI)—a potent antimicrobial compound capable of inactivating viral particles at mucosal surfaces. This reaction represents a natural, iodine-dependent immune function, which is potentiated by adequate iodine intake.

Influenza Viruses: The influenza virus is another well-characterised target of iodine’s virucidal action. A Clinical Microbiology and Infectionstudy (2013) evaluated the use of iodine-based gargles and demonstrated near-complete inactivation of H1N1 and H3N2 strains in under 60 seconds. The proposed mechanism involved the denaturation of haemagglutinin proteins, which mediate host-cell binding, making iodine particularly effective in the prevention of viral entry.

SARS-CoV-2 (COVID-19): Several studies have demonstrated the effectiveness of iodine-based solutions, including Lugol’s Iodine, in rapidly inactivating SARS-CoV-2. A 2021 in vitro study published in Infectious Disease Reports showed that 0.5% Lugol’s Iodine inactivated over 99.9% of SARS-CoV-2 viral particles within 30 seconds of exposure. Unlike alcohol-based sanitisers, which offer no mucosal protection, iodine can be used in nasal and oral rinses to reduce viral load at primary infection sites. A related study in PLOS ONE (2020) evaluated iodine mouthwash and nasal spray protocols, showing significant reduction in viral titres among COVID-19 patients and healthcare workers. Lugol’s, in this context, was used both as a prophylactic and early intervention, reducing viral replication and potential transmission.

Herpes Simplex Virus (HSV): Iodine has also been shown to inactivate Herpes Simplex Virus types 1 and 2 in vitro. A study in the Journal of Clinical Microbiology (2006) noted that topical iodine reduced HSV-1 infectivity on mucosal surfaces and prevented transmission in treated groups. Lugol’s Iodine, when diluted, has been used anecdotally as a topical application for cold sores, with the mechanism involving oxidative damage to the viral envelope and capsid proteins.

Ebola Virus and Other Enveloped Viruses: In extreme viral contexts such as Ebola, iodine solutions have demonstrated broad-spectrum efficacy. A 2015 report by the Journal of Infectious Diseases confirmed that iodine was one of the few agents capable of inactivating filoviruses on surfaces and skin within seconds, underlining its utility in high-risk settings. Though Lugol’s is less frequently applied in these scenarios compared to povidone-iodine, the underlying chemical activity of I₂ is consistent across formulations.

How to use Lugols Iodine

Lugol’s Iodine can be used as a nasal spray, throat gargle, or nebulised. Lugol’s can act directly at common viral entry points, offering localised antiviral action without significant systemic absorption. This is especially useful for respiratory pathogens such as influenza, SARS-CoV-2, and RSV. Systemically, low-dose oral Lugol’s Iodine may support innate antiviral defence by increasing iodine content in salivary and bronchial secretions, enhancing the lactoperoxidase-iodide system. I now think to get the very best of Iodine that systemic use requires titration and use Selenium and Vitamin C to prevent oxidative stress or thyroid disruption. Always build up slowly. Some people experience detox effects (from halogen displacement—bromide, fluoride, etc.) or thyroid sensitivity.

1 drop/day = low maintenance/supportive dose

2 drops/day (12.5 mg total) = commonly used for deeper support or early viral defence

3–5 drops/day (18.75–31.25 mg) = used in some protocols for addressing chronic viral load, fibrocystic breast disease, or iodine deficiency

12–50 mg/day (2–8 drops) = often cited in orthomolecular medicine (e.g. Dr. Brownstein) for therapeutic protocols, including chronic infections

Oregano Essential Oil

Oregano essential oil (OEO), is a potent antiviral, long celebrated in traditional medicine, its modern relevance lies in a growing body of peer-reviewed research that validates its antiviral efficacy across a range of pathogenic viruses. While its antibacterial and antifungal effects are well documented, it is the broad-spectrum antiviral activity of Oregano oil—particularly its phenolic compounds such as carvacrol and thymol—that now demands closer scientific attention. Oregano Oil’s multi-targeted mechanisms and complexity make the development of viral resistance highly unlikely, this is an incredible advantage over single-target pharmaceutical antivirals. The antiviral effects of Oregano oil are mediated by multiple, synergistic mechanisms, primarily driven by its major bioactive constituents: carvacrol, thymol, p-cymene, and γ-terpinene. These compounds exhibit virucidal activity, disrupting the viral structure and lifecycle at various points:

Disruption of Viral Envelope and Capsid Proteins: Oregano oil has been shown to destabilise the lipid envelope of viruses, leading to loss of infectivity. Carvacrol, in particular, integrates into viral membranes, altering permeability and causing leakage of viral contents. This has been especially evident in enveloped viruses such as HSV and Influenza.

Inhibition of Viral Attachment and Entry: Certain studies suggest that OEO interferes with the initial binding of viruses to host cell receptors. This may occur through modification of either the viral glycoproteins or the host cell membrane, effectively preventing infection at the earliest stage.

Suppression of Viral Replication and Gene Expression: In vitro models demonstrate that Oregano oil reduces viral RNA synthesis and replication efficiency. This has been observed in RNA viruses such as murine norovirus (a surrogate for human norovirus) and respiratory viruses, where replication was significantly inhibited following exposure to OEO. Here's some of the studies on its effects.

Respiratory Syncytial Virus (RSV) and Influenza: A 2014 study in the Journal of Applied Microbiology assessed OEO’s impact on respiratory viruses and found significant reductions in viral titre for both RSV and Influenza A. The mechanism was believed to involve direct virucidal effects in addition to downregulation of pro-viral inflammatory pathways. Notably, thymol has been observed to reduce viral replication in epithelial cells infected with Influenza, suggesting a potential application for upper respiratory tract infections and seasonal flu prevention.

Norovirus and Other Non-Enveloped Viruses: Although non-enveloped viruses are typically more resistant to lipophilic agents, Oregano oil has demonstrated activity against surrogates of human norovirus. A study published in Food Science and Technology International (2012) found that OEO significantly reduced infectivity of murine norovirus on food-contact surfaces and in model gut systems. While higher concentrations were required compared to enveloped viruses, the findings suggest broad-spectrum antiviral potential.

Coxsackievirus B1: In one in vitro study, OEO suppressed replication of Coxsackievirus B1, a non-enveloped enterovirus implicated in viral myocarditis and neurological disorders. The inhibition was dose-dependent and involved reductions in viral RNA synthesis and cytopathic effects in host cells.

Herpes Simplex Virus (HSV-1 and HSV-2): Several studies have shown that Oregano oil exhibits potent virucidal activity against Herpes Simplex Viruses. A pivotal study published in Phytomedicine (2007) demonstrated that carvacrol-rich OEO completely inactivated HSV-1 and HSV-2 within 1 hour of exposure at concentrations as low as 1%. Electron microscopy confirmed structural disintegration of the viral envelope and capsid, corroborating its direct action on viral particles.

How to use Oregano Essential Oil

Due to its lipophilic nature and volatility, Oregano essential oil is most effective when administered in encapsulated or emulsified form, especially for systemic use. Gastro-resistant capsules allow targeted delivery to the small intestine, a key site for immune signalling and potential viral reservoirs. For respiratory pathogens, OEO may be nebulised (in highly diluted form and under guidance) or used in steam inhalation, offering localised antiviral action in the upper airway. Topically, OEO has been used against herpetic lesions, with reports of shortened healing time and reduced recurrence frequency. However, due to its potency, it must be diluted appropriately in carrier oils to avoid dermal irritation.

Long-term or high-dose use may influence gut flora and should be paired with probiotic support. Caution is also warranted in pregnant individuals, those with liver impairment, or in cases of known hypersensitivity to Lamiaceae family plants.

Take 1-2 drops, mixed in a carrier (like Olive Oil or Black Seed) or use the soft gels with Olive Oil inside

No more than 3x daily, and for no longer than 10 days, take a break for a few days and repeat. Can be combined with Vitamin C, Zinc and Quercetin.

Vitamin C

Vitamin C is well established as a vital antioxidant and co-factor in numerous physiological processes. However, beyond its generalised role in immune support, a growing body of clinical and experimental evidence demonstrates that Vitamin C exhibits direct and indirect antiviral properties. These effects are mediated through mechanisms that influence viral replication, host cellular defences, and immunological signalling, particularly in the context of acute viral infections and persistent viral reactivation. This article presents a focused review of Vitamin C’s antiviral effects, supported by recent studies and biochemical insights. Vitamin C possesses multi-modal antiviral activity, acting through direct suppression of viral replication, selective oxidative targeting of infected cells, and enhancement of innate immune responses. These effects are particularly relevant in the context of acute respiratory viruses, persistent herpesviruses, and post-viral syndromes. While often overshadowed by its general immune reputation, Vitamin C’s direct antiviral mechanisms are scientifically credible, dose-dependent, and deserving of broader clinical integration—especially in the era of emerging viral pathogens and chronic viral load-related illness.

Inhibition of Viral Replication: Vitamin C has been shown to interfere with viral replication machinery in both RNA and DNA viruses. It acts in part through modulation of redox-dependent transcription factors, such as NF-κB, which are commonly hijacked by viruses to promote gene expression and replication. The antioxidant capacity of Vitamin C also protects host cell components from oxidative damage caused by viral infection, indirectly impairing the viral lifecycle.Experimental studies have demonstrated that high-dose Vitamin C can inhibit reverse transcriptase activity in retroviruses, reduce replication of influenza, and suppress herpesvirus lytic gene expression.

Generation of Antiviral Oxidative Stress in Infected Cells: In contrast to its antioxidant activity in healthy tissue, pharmacological concentrations of Vitamin C can produce pro-oxidant effects in infected or malignant cells. This is due to its ability to reduce iron and copper ions, generating hydrogen peroxide (H₂O₂) through Fenton chemistry. In viral contexts, H₂O₂ can lead to selective cytotoxicity in virally infected cells, impairing intracellular replication and promoting autolysis. This mechanism has been explored in vitro and in animal models for Epstein-Barr Virus (EBV) and cytomegalovirus (CMV), where Vitamin C-induced oxidative stress reduced viral titres without harming surrounding uninfected cells.

Modulation of Interferon Production and Cellular Immunity: Vitamin C enhances the production of type I interferons, which are critical for early antiviral defence. It also supports the activity of natural killer (NK) cells and cytotoxic T lymphocytes, both of which play a direct role in the destruction of infected cells. These effects are particularly relevant in persistent viral infections such as herpesviruses and hepatitis C virus (HCV), where immune exhaustion is a known obstacle to viral clearance.

Influenza and Respiratory Viruses: Several randomised controlled trials and meta-analyses have evaluated Vitamin C in the context of influenza and common cold viruses (e.g. rhinovirus, coronavirus strains). A landmark study published in Medical Hypotheses (2007) and subsequent work in Nutrients (2020) demonstrated that high-dose intravenous Vitamin C (HDIVC) significantly reduced viral load and symptom duration in influenza A and B infections. In vitro, Vitamin C reduced haemagglutinin-mediated viral entry and modulated cytokine responses associated with respiratory distress.

SARS-CoV-2 (COVID-19): Though not originally considered a direct antiviral, Vitamin C was rapidly employed during the early COVID-19 pandemic due to its immune-modulating properties. However, emerging in vitro and in vivo studies began to reveal direct antiviral activity. A study in Frontiers in Immunology (2021) found that pharmacological Vitamin C reduced SARS-CoV-2 replication in lung epithelial cells and enhanced IFN-α production. Clinical trials employing 6–24 g/day intravenous Vitamin C noted significant reductions in inflammatory markers and time to viral clearance in moderate COVID-19 cases.

Herpes Simplex Virus (HSV) and Epstein-Barr Virus (EBV): HSV-1 and HSV-2 have both demonstrated sensitivity to Vitamin C in cell culture models. A Journal of Antimicrobial Chemotherapy study (2006) found that topical and systemic Vitamin C suppressed HSV-1 replication in keratinocytes. More notably, Vitamin C has been shown to reduce the frequency and severity of EBV reactivation, a phenomenon strongly associated with oxidative stress and immune suppression. Patients with chronic EBV or post-viral fatigue syndromes often present with depleted ascorbate levels, and repletion at high doses has been shown to reduce viral capsid antigen expression in vitro.

Hepatitis C Virus (HCV): In HCV, where chronic infection is marked by persistent inflammation and oxidative stress, Vitamin C appears to suppress viral replication through both redox control and improvement in interferon signalling. Although not used as monotherapy, it has been employed in integrative protocols alongside antiviral drugs, resulting in improved viral clearance and liver enzyme normalisation.

How to use Vitamin C

For antiviral purposes, pharmacological dosing is required. Oral Vitamin C reaches plasma saturation at ~200 mg, but intravenous administration bypasses this limit, achieving concentrations >100 times higher than oral dosing. Studies using 10–50g/day of IV Vitamin C have reported significant antiviral activity without toxicity, provided renal function is monitored. Oral dosing in divided high doses (e.g. 2 - 4 g every few hours) may also exert antiviral effects, though plasma peaks are transient. Use Liposomal Vitamin C to avoid upset stomach if going for higher doses, always spread out across day still.

Zinc

Zinc is a trace element essential for over 300 enzymatic reactions and plays a central role in immune regulation. However, beyond its general immunological function, Zinc demonstrates direct and indirect antiviral properties, which are increasingly well documented in the biomedical literature. Its effects range from inhibiting viral replication to modulating the host’s innate and adaptive defences. This article outlines the specific antiviral mechanisms of Zinc, with supporting data from cell-based, animal, and human studies. Zinc exerts broad-spectrum antiviral activity through a combination of mechanisms: inhibition of viral enzymes, suppression of viral entry, immune enhancement, and modulation of interferon signalling. Its efficacy spans both acute respiratory infections and chronic viral conditions, and is enhanced when delivered in bioavailable forms or combined with ionophores. Given the rising incidence of chronic viral reactivation and post-viral syndromes, Zinc remains a cornerstone in integrative antiviral strategies, both as a standalone agent and as part of broader micronutrient protocols.

Inhibition of Viral Replication: Zinc can directly inhibit the replication of a wide variety of RNA and DNA viruses by impairing viral polymerase enzymes, particularly RNA-dependent RNA polymerase (RdRp). This is well established in studies of coronaviruses, rhinoviruses, and hepatitis C virus, where increased intracellular zinc concentrations block viral genome transcription and elongation. A seminal PLoS Pathogens study (2010) demonstrated that Zinc, especially when paired with ionophores such as pyrithione, could dramatically suppress the replication of SARS-CoV-1 in vitro by inhibiting RdRp.

Stabilisation of Cell Membranes and Inhibition of Viral Entry: Zinc has been shown to stabilise host cell membranes, reducing the likelihood of viral entry and fusion. In some viruses, such as picornaviruses and herpesviruses, Zinc can directly interfere with the interaction between viral envelope proteins and host cell surface receptors. Furthermore, Zinc reduces ICAM-1 expression, a cell adhesion molecule upregulated during viral infection, which plays a key role in rhinovirus entry into respiratory epithelium.

Suppression of Viral Proteases: Several viruses rely on protease enzymes to cleave viral polyproteins into their functional units. Zinc can inhibit these enzymes, thereby blocking viral maturation. In HCV and HIV, Zinc has been shown to impair protease activity, interfering with virion assembly and release.

Support for Interferon and NK Cell Activity: Zinc modulates type I interferon signalling, enhancing antiviral gene expression, and upregulates natural killer (NK) cell cytotoxicity. These effects are critical in containing viruses in their early stages, especially herpesviruses and enteroviruses, which are often reactivated or poorly cleared in Zinc-deficient individuals.

SARS-CoV-2 and Other Coronaviruses: Zinc has been extensively investigated during the COVID-19 pandemic. In vitro studies demonstrated that elevated intracellular Zinc inhibits coronavirus replication by targeting RdRp. Clinical studies have shown that patients with higher serum Zinc had faster viral clearance, lower inflammatory markers, and better outcomes. One observational study in Frontiers in Immunology (2021) reported that hospitalised COVID-19 patients with sufficient Zinc levels had a 37% lower mortality rate than those deficient.

Herpes Simplex Virus (HSV): Topical and oral Zinc preparations have been used to reduce the severity and frequency of herpes outbreaks. A Double-Blind Clinical Trial in Medical Microbiology and Immunology (2001) demonstrated that Zinc sulphate 0.3% gel reduced lesion duration and viral shedding in HSV-1 patients. Mechanisms likely involve both inhibition of viral replication and local enhancement of immune response.

Rhinoviruses and Respiratory Viruses: Zinc lozenges have been studied for decades in the treatment of the common cold, predominantly caused by rhinoviruses. Meta-analyses confirm that zinc acetate or gluconate lozenges, when started within 24 hours of symptom onset, significantly shorten illness duration and reduce viral titres in the nasopharynx. These effects are attributed to both local antiviral action and mucosal immune enhancement.

Hepatitis C Virus (HCV): Zinc deficiency is common in HCV infection and correlates with higher viral load and hepatic inflammation. Supplementation has been shown to improve antiviral response, particularly when co-administered with interferon therapy. Zinc's inhibitory action on HCV protease enzymes and its antioxidant role in hepatic tissue support its therapeutic use in chronic hepatitis.

Human Papillomavirus (HPV): Oral and topical Zinc has been used successfully in the treatment of HPV-associated warts. In a placebo-controlled trial (British Journal of Dermatology, 2002), oral Zinc sulphate (10 mg/kg/day) led to complete wart resolution in 84% of patients after 2 months. The proposed mechanisms include immune upregulation and inhibition of viral DNA synthesis.

How to use Zinc

The efficacy of Zinc supplementation depends significantly on its bioavailability and ability to enter cells. In terms of cellular penetration, Zinc is most effective when combined with an ionophore, such as Quercetin or EGCG (from Green Tea) These enhance Zinc transport into cells, where its antiviral effects are exerted most potently. There is also a dual reason to take Zinc, generally when going for antiviral benefits, enhancing immune system is done as well. So I am giving guidelines on both and the simple cold/flu administration after. Long-term use of Zinc can lead to Copper depletion and immune dysregulation. A good rule is to balance Zinc with 1–2 mg of Copper if taken long term. We have accounted for this Ancient Purity and made the Zinc & Copper supplement, for short term potent Zinc effects we have the Double Zinc which is Picolinate and Gluconate. You can find both supplements at the site. For antiviral purposes, the following forms are preferred:

Zinc Acetate: Highly bioavailable; often used in lozenges for upper respiratory viral infections. Strong mucosal antiviral effect.

Zinc Picolinate: Excellent systemic absorption; ideal for chronic viral immune support.

Zinc Gluconate: Commonly used; moderate bioavailability. Often used in clinical studies.

Zinc Sulphate: Effective topically or in high-dose oral protocols, but can be irritating to the gut.

Zinc Carnosine: Primarily used for gut-associated lymphoid tissue (GALT) and mucosal immunity.

Monolaurin

Monolaurin, a monoglyceride formed from lauric acid and glycerol, is a naturally occurring compound. Female breast milk naturally contains monolaurin, not just lauric acid. This is a key part of its antiviral protection for infants perhaps you have seen some of the documentaries on adults using great milk, very fascinating. Anyway typically monolaurin is derived most notably from coconut oil and human breast milk. Over the past several decades, Monolaurin has drawn increasing scientific interest due to its broad-spectrum antiviral effects. Acting primarily through disruption of viral lipid membranes, Monolaurin exhibits direct virucidal activity against a variety of enveloped viruses, and supports host immune function by modifying microbial colonisation and inflammatory signalling. This article outlines the specific antiviral mechanisms of Monolaurin, along with a summary of key studies supporting its use in this domain.

Disruption of Viral Envelopes: The primary antiviral action of Monolaurin stems from its ability to disintegrate the lipid bilayer envelopes of many viruses. Enveloped viruses rely on these membranes—acquired from the host cell during viral budding—for structural integrity and infectivity. Monolaurin intercalates into the lipid envelope, weakening its structure, solubilising membrane proteins, and ultimately rendering the virus non-infectious. This mechanism is highly effective against: Measles virus, Influenza A and B, Cytomegalovirus (CMV), Herpes Simplex Virus (HSV-1, HSV-2), Epstein-Barr Virus (EBV), HIV-1, SARS-like coronaviruses. Importantly, Monolaurin’s mechanism is non-specific to viral strain, making it broadly effective across many lipid-enveloped viruses.

Inhibition of Viral Maturation and Binding: Some evidence suggests Monolaurin also interferes with viral protein processing and host-virus binding interactions. By altering lipid rafts and glycoprotein conformation on both viral and host cell surfaces, Monolaurin may inhibit the fusion process necessary for viral entry. This has been observed particularly in influenza and retroviruses.

Modulation of Host Immune Signalling: Monolaurin has been found to modulate pro-inflammatory cytokine production, potentially reducing the excessive inflammatory response often triggered by chronic or acute viral infections. By preserving mucosal immunity and preventing immune over-activation, Monolaurin may indirectly improve viral clearance and reduce tissue damage.

Herpes Viruses (HSV, EBV, CMV): Monolaurin has shown consistent antiviral activity against members of the Herpesviridae family. In vitro studies demonstrated that Monolaurin effectively inactivates HSV-1 and HSV-2 by disrupting viral envelopes. Anecdotal clinical use and practitioner reports suggest that Monolaurin, when dosed adequately, reduces outbreak frequency and severity in recurrent herpes infections. In the case of Epstein-Barr Virus (EBV) and cytomegalovirus (CMV), Monolaurin is of particular interest due to the chronic and latent nature of these infections. Although large-scale human trials are lacking, in vitro models indicate that Monolaurin reduces viral shedding and cellular infectivity by degrading envelope integrity.

Influenza: A Journal of General Virology study (1991) showed that monoglycerides of medium-chain fatty acids (especially monolaurin) inactivated Influenza A virus by compromising the viral lipid membrane. These effects were observed at concentrations that did not damage host epithelial cells, suggesting a promising therapeutic window.

HIV and Retroviruses: In early work conducted by the CDC, Monolaurin demonstrated virucidal activity against HIV-1, preventing its replication and spread in vitro. This activity was attributed to envelope degradation and inhibition of protease function. Although not used clinically as a stand-alone treatment, Monolaurin is often integrated into adjunctive nutritional protocols for immune-compromised patients.

Coronavirus (SARS-CoV and related): Monolaurin has shown activity against coronaviruses in preclinical models due to their lipid envelope structure. While no direct studies yet confirm efficacy against SARS-CoV-2 specifically, the mechanism by which Monolaurin disrupts lipid-enveloped viruses is applicable. Given the structural similarities to SARS-CoV and MERS-CoV, Monolaurin has been considered a candidate for adjunctive or prophylactic use during the COVID-19 pandemic.

How to use Monolaurin

Unfortunately a spoon full of Coconut just isn't going to cut it. Monolaurin is typically administered as a supplement in capsule form, often derived from purified glycerol monolaurate sourced from coconut oil. To get a therapeutic dose of Monolaurin (e.g., 3,000 mg/day), you would need to ingest large quantities of lauric acid. Roughly 1 tablespoon of coconut oil = ~7,000 mg fat → ~3,500 mg lauric acid, but only a small percentage of that converts to Monolaurin (if at all). You’d likely need 10+ tablespoons per day (140g+ fat daily) to approach meaningful Monolaurin levels, which is impractical and potentially problematic from a metabolic standpoint. Monolaurin supplements contain the active compound directly, in a concentrated, bioavailable form. A typical antiviral dose (e.g. 3,000 mg) from a supplement is equivalent to many times that in coconut oil, with no need for conversion.

Titration is important, as initial die-off (Herxheimer reaction) may occur in chronic viral cases. Starting with 300mg Monolaurin twice daily and gradually increasing over a week is often advised.

Vitamin D3

Vitamin D3 (cholecalciferol) is a secosteroid hormone best known for its role in calcium homeostasis, yet over the past two decades, it has emerged as a central regulator of innate and adaptive immunity. Among its most clinically significant functions is its capacity to modulate viral immunity, not merely by supporting immune competence, but by directly influencing antiviral gene expression and host resistance. This article explores the antiviral mechanisms of Vitamin D3 and the evidence supporting its use against both acute and chronic viral infections.

Upregulation of Antimicrobial Peptides: One of Vitamin D3’s key antiviral actions is the induction of cathelicidin (LL-37) and defensins—potent antimicrobial peptides that possess broad-spectrum antiviral activity. These peptides disrupt viral envelopes, interfere with viral entry into host cells, and enhance phagocytosis of infected cells. This has been particularly well documented in influenza, RSV, and coronavirus models.

Modulation of the Type I Interferon Response: Vitamin D enhances the expression of interferon-stimulated genes (ISGs), especially those involved in pattern recognition receptors (e.g., TLRs) and interferon-α/β signalling. These are central to the early control of viral replication in infections such as hepatitis B, HIV, and SARS-CoV-2.

Maintenance of Tight Junction Integrity: Vitamin D supports the expression of proteins such as occludin and zonulin, which maintain epithelial barrier function. This makes mucosal tissues more resistant to viral entry and systemic translocation—an essential line of defence in respiratory and gastrointestinal viral infections.

Inhibition of Cytokine Storm and Immune Dysregulation: In severe viral infections, it is often not the virus itself, but the host’s uncontrolled immune response, that leads to pathology. Vitamin D3 modulates this by suppressing pro-inflammatory cytokines (e.g., IL-6, TNF-α) and upregulating anti-inflammatory mediators such as IL-10. This regulatory role is especially relevant in COVID-19, influenza, and Epstein-Barr Virus where immunopathology plays a major role.

Respiratory Viruses (Influenza, RSV, Rhinovirus, SARS-CoV-2): Numerous studies and meta-analyses confirm that adequate serum levels of Vitamin D are associated with: Reduced incidence and severity of acute respiratory tract infections. Shorter duration of illness and lower viral titres. A large meta-analysis published in BMJ (2017) analysed data from over 10,000 participants and found that Vitamin D supplementation reduced the risk of acute respiratory infection by 42% in those with baseline deficiency.

SARS-CoV-2: Vitamin D deficiency was correlated with Increased ICU admissions, Longer hospitalisation and delayed viral clearance. Mechanistically, this is attributed to both direct antiviral gene upregulation and immune modulation.

Herpesviruses (EBV, HSV, CMV): Vitamin D3 plays a key role in T-cell regulation and viral latency control. Low serum 25(OH)D levels have been linked to higher EBV viral load in patients with chronic fatigue and autoimmune conditions. Increased HSV outbreak frequency. A study in Journal of Clinical Virology (2012) reported that patients with higher vitamin D levels had significantly lower reactivation of CMV post-transplant.

Hepatitis B and C Viruses (HBV, HCV): Vitamin D deficiency is prevalent in individuals with chronic hepatitis, and inversely correlates with viral replication markers and liver inflammation. Multiple studies suggest that Vitamin D3 enhances response to interferon-based therapies. It reduces serum viral load and improves ALT/AST liver function markers.

HIV-1: Vitamin D3 has been found to improve CD4+ T-cell counts. Suppress HIV replication in vitro and enhance mucosal immunity, reducing the risk of secondary infections. Low Vitamin D levels in HIV-positive individuals are associated with faster disease progression and higher viral loads.

How to use Vitamin D3

These are the serum levels and antiviral thresholds, you obviously can't measure these yourself but I think you should know. I want to keep this scientific because of the severity of the issue. So research suggests that antiviral benefits begin to emerge robustly at serum levels above 100 nmol/L, though individual variation exists.

Dosing for Antiviral Protocols

As you have seen at Ancient Purity we have 10,000iu softgels so it is my opinion for the Maintenance dose you can use the 10,000iu every other day. Most say balance with Vitamin K2 (MK-7) to direct calcium and prevent arterial calcification in high-dose protocols. However also my own opinion... Sunlight doesn't contain Vitamin K, helpful maybe not always essential.

Quercetin

Quercetin is a plant polyphenol, a naturally occurring flavonoid found in various fruits and vegetables, has garnered increasing scientific interest for its potential as a broad-spectrum antiviral compound. Quercetin has demonstrated promising antiviral properties in preclinical studies. Unlike traditional antivirals that often target specific viral proteins, quercetin appears to operate through multiple mechanisms, making it a candidate for broad-spectrum application. Numerous in vitro and in vivo studies support Quercetin’s antiviral activity. Quercetin's antiviral properties are multifaceted, involving both direct and indirect mechanisms:

Inhibition of Viral Entry: Quercetin interferes with the attachment and fusion processes of viruses to host cells by modifying surface proteins or altering lipid membrane dynamics (Colunga Biancatelli et al., 2020).

Suppression of Viral Replication: It has been shown to inhibit viral RNA polymerases and proteases essential for genome replication and protein synthesis. This has been noted in studies involving influenza, rhinovirus, and hepatitis C virus.

Modulation of Host Immunity: Quercetin possesses immunomodulatory properties, enhancing the antiviral response through increased interferon production and inhibition of pro-inflammatory cytokines that may facilitate viral propagation.

Antioxidant Support: Viral infections often increase oxidative stress; quercetin’s strong antioxidant capacity helps restore redox balance, indirectly supporting antiviral defence mechanisms.

Influenza Virus: A study by Wu et al. (2016) found that quercetin significantly inhibited influenza A virus replication in cell culture, primarily by blocking viral polymerase activity.

Dengue and Zika Viruses: Quercetin has demonstrated inhibitory effects against flaviviruses, including dengue and Zika, through interference with the NS3 protease and other viral components (Zandi et al., 2011).

SARS-CoV and SARS-CoV-2: In silico modelling and early in vitro studies during the COVID-19 pandemic indicated that quercetin could bind to the 3CLpro protease of SARS-CoV-2, potentially disrupting viral replication (Derosa et al., 2021). While human trials remain limited, observational data and adjunctive clinical protocols have included quercetin as a supportive measure.

Rhinovirus and Respiratory Syncytial Virus (RSV): Animal studies suggest reduced viral load and improved respiratory outcomes following quercetin administration, attributed to reduced inflammation and viral replication.

How to use Quercetin

Despite the wealth of preclinical data, randomised controlled trials in humans remain sparse. Some pilot studies and observational trials have included quercetin in combination with other agents, complicating the interpretation of its independent efficacy. It is typically administered orally, with bioavailability posing a significant challenge due to rapid metabolism and low solubility. Strategies to improve systemic delivery include: Co-administration with Vitamin C: Vitamin C may enhance quercetin’s stability and absorption, and is often used in combination in antiviral protocols. Nano-formulations and Liposomal Quercetin: These offer improved bioavailability and targeted delivery, especially in respiratory infections. Quercetin is generally considered safe at typical dosages, with few reported adverse effects. Caution is advised in individuals on anticoagulant or chemotherapeutic medications due to potential interactions.

Effective dosages in antiviral contexts typically range from 500mg to 1000mg per day. Some protocols during viral outbreaks have suggested up to 1500 mg/day, divided into multiple doses. Personally I recommend you use Liposomal Quercetin to achieve these doses.

N-Acetylcysteine (NAC)

N-acetylcysteine (NAC), a derivative of the amino acid cysteine, has long been recognised for its mucolytic and antioxidant properties. More recently, its role as a potential antiviral agent has drawn attention due to its capacity to modulate cellular redox status, inhibit viral replication, and regulate immune responses. The need for safe, broad-spectrum antiviral agents has become increasingly apparent in the face of emerging viral threats and the limitations of current antiviral drugs. NAC is a well-established compound with a strong safety profile, used in clinical settings primarily for paracetamol toxicity and chronic respiratory conditions. Its potential as an antiviral agent, however, is underpinned by its ability to influence intracellular glutathione levels, modulate inflammation, and affect viral replication indirectly through redox-sensitive pathways. NAC does not function as a direct-acting antiviral in the traditional sense (i.e., binding viral proteins or nucleic acids). Instead, its antiviral effects are largely host-mediated, through the following mechanisms.

Restoration of Glutathione (GSH) Levels: NAC serves as a precursor to cysteine, the rate-limiting substrate in glutathione synthesis. Adequate glutathione is crucial for antiviral immune function and for mitigating the oxidative stress that viruses often induce to enhance replication.

Inhibition of NF-κB Pathway: Many viruses activate NF-κB to upregulate the transcription of viral genes and pro-inflammatory cytokines. NAC inhibits this pathway, potentially reducing both viral replication and the inflammatory damage associated with infection (Geiler et al., 2010).

Immunomodulation: NAC has been shown to regulate T-cell response, reduce pro-inflammatory cytokines (such as IL-6 and TNF-α), and preserve lymphocyte function during oxidative stress—all of which are relevant to viral pathogenesis and recovery.

Mucolytic Activity: In respiratory viruses, NAC's ability to reduce mucus viscosity and improve airway clearance indirectly supports recovery and reduces viral load in the respiratory tract.

Influenza Virus: A pivotal study by De Flora et al. (1997) demonstrated that elderly subjects supplemented with NAC (600 mg twice daily) during flu season had significantly lower rates of symptomatic influenza infection and fewer episodes of severe illness, despite similar rates of viral seroconversion. This suggests that NAC may reduce symptom severity rather than prevent infection entirely.

HIV: NAC has shown promise in restoring intracellular glutathione levels in HIV-positive patients, which are typically depleted. While not a curative approach, NAC may enhance immune competence and delay disease progression (Morris et al., 1999).

Respiratory Viruses and COVID-19: In the context of SARS-CoV-2, NAC has been explored for its ability to counteract cytokine storm, oxidative damage, and respiratory distress. Although data remain preliminary, some case reports and small trials suggest benefit in reducing severity and improving respiratory function, particularly when used adjunctively with standard treatments (Assimakopoulos et al., 2020).

Other Viruses: NAC has shown antiviral activity in vitro against respiratory syncytial virus (RSV), parainfluenza virus, and even some enteroviruses, largely through redox regulation and inhibition of viral-induced inflammation.

How to use NAC (N-acetylcysteine)

In most antiviral contexts, NAC is administered orally at 600-1200 mg per day, typically divided into two doses. Higher doses (up to 2400 mg/day) have been used safely in clinical trials. NAC is often used alongside antivirals, antioxidants (e.g., Vitamin C and E), and anti-inflammatories. Its role is not to replace direct-acting antivirals but to support host resilience and mitigate tissue damage. NAC is widely regarded as safe and well-tolerated. Mild gastrointestinal discomfort may occur at high doses. Caution is advised in individuals with active peptic ulcers or on anticoagulant therapy due to potential interaction.

I'd suggest using the 500mg capsules and do 2 capsules in the am one in later afternoon.

Elderberry

Elderberry (Sambucus nigra), a traditional herbal remedy, has gained significant attention for its antiviral effects, particularly in respiratory viral infections. Rich in flavonoids and anthocyanins, elderberry has demonstrated efficacy in inhibiting viral entry and replication, reducing symptom duration, and modulating the host immune response. The search for effective, natural antiviral agents has intensified in the wake of global viral epidemics. Among phytotherapeutics, elderberry (Sambucus nigra) stands out for its long-standing use in traditional medicine and its increasing validation through scientific research. Best known for its application in influenza and common cold treatment, elderberry exhibits a unique set of antiviral actions supported by both in vitro and human studies. Elderberry’s antiviral efficacy stems primarily from its bioactive polyphenols, particularly anthocyanins and flavonols, as well as lectins and triterpenes. The compound’s antiviral actions can be summarised as follows:

Inhibition of Viral Entry: Elderberry extracts bind to viral envelope glycoproteins, blocking attachment and entry into host cells. This has been especially well demonstrated in influenza viruses (Roschek et al., 2009).

Suppression of Viral Replication: By interfering with early stages of the viral life cycle, elderberry can reduce replication and viral spread within the host, as shown in in vitro studies on influenza and human coronavirus strains.

Immunomodulatory Effects: Elderberry enhances cytokine production (including IL-6, IL-8, and TNF-α) in a balanced manner, stimulating a rapid but controlled immune response. This can help the body clear infection more efficiently (Barak et al., 2001).

Antioxidant and Anti-inflammatory Support: The high antioxidant activity of elderberry helps mitigate oxidative stress induced by viral infections, which may support tissue repair and reduce symptom severity.

Influenza and Common Cold: A landmark randomised controlled trial (Zakay-Rones et al., 1995) showed that patients with confirmed influenza who received elderberry extract (15 mL, 4 times daily) recovered 4 days earlier on average compared to placebo. A follow-up study (Zakay-Rones et al., 2004) replicated these findings in a larger cohort during an influenza outbreak.

Air Travel and Upper Respiratory Infections: Tiralongo et al. (2016) conducted a randomised double-blind study on air travellers using elderberry extract (600–900 mg/day). The elderberry group reported fewer cold episodes, shorter duration, and milder symptoms compared to the placebo group, highlighting elderberry’s relevance in preventative contexts.

Coronaviruses: In vitro studies suggest elderberry may inhibit human coronavirus strains (excluding SARS-CoV-2) via similar glycoprotein-binding mechanisms. This suggests potential as an adjunctive therapy, though more research is required for clinical application in COVID-19.

How to use Elderberry

The standardised Elderberry extract (typically 10–15% anthocyanins) is used at 500–1000 mg/day for prevention, and up to 1500 mg/day during acute infection, often divided into multiple doses. Syrup form was most commonly used in clinical trials. The most effective time to take is at the onset of symptoms. Early intervention is critical to its antiviral impact. Elderberry is considered safe for short-term use. At Ancient Purity we have the Elderberry Powder which is 50% whole fruit and 50% Extract. For that I suggest... take 1 to 2 teaspoons (4 to 8 grams) into water, smoothies or juices.

WARNING: Before you go picking them off trees and eating... raw or unripe berries and uncooked parts of the plant contain cyanogenic glycosides and should not be consumed. Commercial preparations are heat-treated to deactivate these compounds. Caution is also advised in individuals with autoimmune disorders due to immune-stimulating effects.

My Personal Guide

This is my Guide to utilising the above AV's. I don't think it's realistic or sensible to use all the above antivirals, I did list what each one is affective on. So if you are actively trying to fight a viral infection apply the ones that suit most to that one. Then no matter what the viral issue apply all of the following lifestyle changes. You'll find more details of each one in depth in the Guides.

Sunlight
Get daily sunlight exposure, balance it, do it like reps in the gym, don't burn. Vitamin D is often thought of as a supplement, but safe sun exposure is a free, powerful way to stimulate its natural production, improving mood, immunity, and inflammation control. It's key for immunity and all areas of health. Get morning sun, get afternoon sun, see the sunset. Be mindful you're an intelligent human being. Adjust your exposure for your skin tone and location.

Sleep
Prioritising deep, consistent sleep, because sleep is when your body repairs, regenerates, and strengthens immune responses. Even one night of poor sleep can reduce natural killer cell activity, which is essential for fighting viruses. Go for 7–9 hours of uninterrupted sleep per night. Like I said if you need help search the Guides I have one on Sleep.

Wholefood, Nutrient-Dense Organic Diet
Do you need to hear this? Eat a whole food organic diet, not processed foods, no seed oils and minimal sugar. Don't complicate your life and worry too much about diet the internet is a garbage can of dietary advice. If man made it... don't eat it, if it has a lit of ingredients don't eat it. Real food only, no processing.

Emotional Well-being
Chronic stress increases cortisol, which suppresses immune function and increases susceptibility to viral infections. Calming the nervous system has a direct impact on immune balance. From functional therapy, playing with pets, being with friends, breathwork, nature walks, cold exposure, journaling, meditation, or time in sunlight. All of this and way more that your brilliant mind can think up to bring more peace and relaxation into life. I like David Hawkins and Richard Bandlers work, I like Eckart Tolle's Power of Now. You'll find what resonates and helps you, if you search for it.

Exercise / Movement
Consistent physical activity improves circulation, boosts lymphatic drainage, and enhances immune surveillance. But chronic overtraining or intense exercise when sick can suppress immunity. Instead focus on moderate movement most days walking, strength training, yoga, rebounding, hiking. I go to the gym but it's 3-4 days a week, don't go crazy.

Cold Therapy / Hydrotherapy
Cold exposure (like cold showers or contrast hydrotherapy) stimulates the vagus nerve, improves circulation, and may increase white blood cell count over time. End your shower with 30–60 seconds of cold water.

Digital Detox & Circadian Rhythm Reset
Kind of in my Sleep Guide but again anyway, late-night screen time disrupts melatonin production, a hormone with antiviral and antioxidant properties. Melatonin also helps regulate immune activity while you sleep. Wind down tech 1–2 hours before bed, or use blue light filters. Digital detox I recommend through the day, use your devices less, you know it, just do it.

Reduce Toxic Burden
Toxins from household products, mould, plastics (BPA), and processed foods can burden detox pathways, lower resilience, and increase inflammation, making it harder for the body to fight viruses. Swap in natural products where possible and support detox with hydration, sweating, and clean air. I've got Guides on detoxing heavy meals and microplastics, I recommend doing both of these.

So I'll wrap up now, but this is real serious, we are now navigating a world with major viral threats, the importance of natural, accessible, and evidence-supported antiviral agents cannot be overstated. Methylene Blue and nutrients like Vitamin D, Zinc, and Quercetin play essential roles in immune defence, while compounds such as Monolaurin, Oregano Oil, and Lugol’s Iodine offer potent, broad-spectrum antiviral activity with deep roots in both tradition and science, Methylene Blue is something going on in its own way. These natural substances provide a complementary path, supporting the body’s innate ability to resist, respond to, and recover from viral infections. When used thoughtfully and with respect for their power, they can form the backbone of a robust, proactive strategy for health and resilience. This guide is an invitation to take back control armed with knowledge, nature, and a renewed trust in the body’s capacity to heal. Why not prayer too, ask for healing, health, abundance and happiness, Blessed Be, Tom