Our natural herbal supplement (Viral +C (+Covid), is designed to support the body’s immune response against various viruses, including Covid, Rotavirus, RNA viruses, TB, and Herpes. Its mechanism includes naturally assisting the body to block ACE2 receptors, potentially impeding viral replication.

This Viral Plus C capsule does not ensure or claim to cure or prevent Coronaviruses, SARS viruses, or other related viruses. It is intended to build immunity. The information below is based on worldwide research.

Why this Herbal Supplement is so effective:

Our Herbal Viral Plus+C (+Covid) supplement is a thoughtfully crafted natural blend aimed at reinforcing the body’s immune response against a spectrum of viruses, with a focus on Covid, Rotavirus, RNA viruses, TB, Herpes, and Pulmonary Fibrosis. By strategically blocking ACE2 receptors, it endeavours to impede the replication of viruses, contributing to overall immune resilience. It’s crucial to note that while the supplement doesn’t claim to cure or prevent specific viral infections, it is rooted in extensive global research and serves as a proactive measure for immune system fortification.

This comprehensive formula goes beyond immune support. It actively elevates glutathione levels, crucial for antioxidant defense and detoxification processes. The modulation of TH1 & TH2 cells, along with support for TH3 helper cells, aims to create a balanced immune response. The inclusion of a protease inhibitor and acting as a TH17 & NF Kappa B-Blocker showcases the supplement’s multifaceted approach. Addressing conditions such as Coxsackie Virus, Endothelial Dysfunction, and Chronic Fatigue Syndrome underscores its versatility.

Furthermore, the supplement taps into the body’s inherent abilities, serving as a tonic to promote immune function and support vital processes. As a strategic response to the ongoing research, it aligns with the understanding that a robust immune system is pivotal in countering viral threats. In essence, the supplement acts as a partner in bolstering the body’s resilience, offering immune support while navigating the complexities of viral challenges.

Research on Coronavirus:

Why do men have more severe Covid-19 disease and a higher fatality rate than women?

We currently know that men have more severe Covid-19 disease and a higher rate of fatality compared to women, and we also know that children under age 10 seem extremely resistant.

• Before age 10, in normal conditions, neither girls nor boys have increased androgens. The first androgensstart to appear during a period called adrenarche, around age 8, but those androgens produced by the adrenal glands are not very potent. After age 10 comes puberty, and androgens rise, produced by the gonads – increasing hair density in some areas, as well as oily scalp and acne. Androgen production peaks during adulthood and decreases in the elderly. After menopause, women start to overexpress androgens, because of the huge drop of estrogen (female hormone), and there is an increase in facial hair, and also a decrease in scalp hair density.

• Taken together, this could help to explain why we are seeing more severe and fatal Covid-19 cases in men, with a lower rate for women and very few for young children.

• Research links two well-known scientific facts. First, that SARS-CoV-2 needs its spikes to be primed by the TMPRSS2 protease. Second, the TMPRSS2 gene has only one known gene promoter, the androgen receptor. The gene requires androgen hormones to bind to the androgen receptor, so the cell can initiate the transcription of the TMPRSS2 gene to produce the protease—a cell-surface protein that “eats” other proteins. Without this protease, host cells are not infected with SARS-CoV-2 because the virus spikes cannot bind to ACE2, a receptor implicated in Covid-19 and severe acute respiratory syndrome. The protease “eats” the spikes so they can connect to the ACE2. So, more androgen activity means more proteases, which we think leads to more severe infection.
• Benign prostate enlargement is caused by a very potent androgen hormone, called DHT. This is the most potent natural androgen, and it binds with great affinity to the androgen receptor—making it express proteins like TMPRSS2, which has been studied for decades in prostate health and prostate cancer research and is now known to open the door to novel coronavirus.
• Women also produce DHT and testosterone, though at much lower levels than men. However, due to ovary diseases such as PCOS or ovary adenomas, women can produce very high levels of male hormones. We know PCOS is related to obesity and diabetes, so women with these conditions and post-menopausal women are likely more susceptible to severe infections, following the androgen vulnerability rationale.

How the covid virus attaches to ace to receptors:

• Virus Structure: The Covid-19 virus, or SARS-CoV-2, has spike proteins (S-proteins) on its surface. These spike proteins are crucial for the virus’s ability to interact with host cells.
• ACE2 Receptors: ACE2 receptors are proteins found on the surface of certain cells, especially in the respiratory system, lungs, and other organs. These receptors play a significant role in regulating blood pressure and inflammation.
• Attachment Process: The spike proteins on the virus bind specifically to ACE2 receptors on the surface of host cells. Binding is facilitated by the receptor-binding domain (RBD) of the spike protein.
• Conformational Changes: Upon binding, conformational changes, occur in the spike protein. These changes are crucial for the virus to enter the host cell.
• Viral Entry: The attachment triggers the entry of the virus into the host cell. The virus may enter the cell through endocytosis, a process in which the cell engulfs the virus in a vesicle.
• Fusion and Release: Subsequently, the viral membrane fuses with the host cell membrane, releasing the viral genetic material (RNA) into the host cell.
• Replication and Spread: The host cell’s machinery is then hijacked to replicate the viral genetic material and produce new virus particles. These new viruses can go on to infect more cells, leading to the spread of the infection.

Understanding this mechanism is crucial for developing targeted therapeutic approaches to interfere with the virus’s ability to enter and infect host cells.

TMPRSS2 Protease connection to Covid:

TMPRSS2 (Transmembrane Protease, Serine 2) is a protein-coding gene that encodes a serine protease. This enzyme is involved in the activation of certain proteins through cleavage, and its expression is detected in various tissues throughout the body. TMPRSS2 is particularly significant in the context of viral infections, including its connection to the severity of Covid-19.

TMPRSS2 in Males and Females:

• Males: TMPRSS2 is expressed in various tissues in males, including the prostate, lung, and other organs. In males, TMPRSS2 plays a role in the activation of proteins associated with normal physiological functions. It is prominently studied in the context of prostate cancer, where TMPRSS2 gene fusions are often observed.
• Females: TMPRSS2 is also expressed in females, but its levels are generally lower than in males. In females, TMPRSS2 may play a role in normal cellular processes, but it is less explored compared to its implications in males.

Connection to Severe Covid-19:

• Androgen Receptor and Hormonal Influence: TMPRSS2 expression is regulated by the androgen receptor, a receptor for male sex hormones, such as testosterone. Studies have shown that TMPRSS2 is upregulated in the presence of androgens, which are more abundant in males. This upregulation of TMPRSS2 in males is believed to be one factor contributing to the increased severity of Covid-19 in men compared to women.
• SARS-CoV-2 Entry Mechanism: SARS-CoV-2, the virus that causes Covid-19, enters human cells by binding to the ACE2 receptor on the cell surface and then undergoing priming or activation by proteases like TMPRSS2. The androgen receptor-driven upregulation of TMPRSS2 in males is thought to facilitate increased viral entry and infection.
• Potential Therapeutic Targets: The androgen-driven regulation of TMPRSS2 suggests that hormonal factors may influence the severity of Covid-19. Targeting TMPRSS2 or modulating androgen levels are being explored as potential therapeutic strategies to mitigate the severity of the disease, especially in males.

Understanding the role of TMPRSS2 in the severity of Covid-19 provides insights into potential gender-based differences in susceptibility and outcomes. The hormonal regulation of TMPRSS2 expression underscores the need for further research to explore targeted interventions and treatment approaches that consider these factors.

What is the difference between normal flu and Covid-19?

While both influenza (flu) and COVID-19 are respiratory illnesses caused by different viruses, there are some key differences between the two. Here are some distinctions:

• Difference Between Flu and Covid-19: Causative Viruses: Flu is caused by influenza viruses (types A and B). COVID-19 is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2).
• Symptoms: Flu symptoms include fever, cough, sore throat, runny or stuffy nose, body aches, headaches, fatigue, and sometimes vomiting and diarrhoea. Covid-19 symptoms encompass fever, cough, shortness of breath, fatigue, body aches, headache, sore throat, loss of taste or smell, congestion or runny nose, nausea or vomiting, and diarrhoea. Symptoms can vary from mild to severe.
• Incubation Period: The incubation period for the flu is usually shorter, typically 1-4 days after exposure. For Covid-19, it is generally longer, ranging from 2 to 14 days after exposure.
• Spread and Transmission: The flu primarily spreads through respiratory droplets and by touching surfaces with the virus. Covid-19 is primarily transmitted through respiratory droplets and can also spread by touching contaminated surfaces.
• Testing and Diagnosis: Rapid flu tests are available to diagnose influenza. Covid-19 is diagnosed using PCR and antigen tests.
• Complications: Flu complications may include pneumonia, bronchitis, sinus infections, and ear infections. Severe Covid-19 complications include acute respiratory distress syndrome (ARDS), blood clotting issues, organ failure, and potential long-term effects.

It’s crucial to recognize that flu and Covid-19 symptoms can overlap, making accurate identification challenging based solely on clinical presentation.

Pulmonary Fibrosis and COVID-19

Pulmonary fibrosis is a lasting lung condition that can occur after recovering from Covid-19. When you have Covid-19, the virus can cause inflammation in your lungs, leading to the development of scar tissue over time. This scarring, known as fibrosis, alters the normal structure of the lungs and can make it harder for them to work properly.

People who had severe cases of Covid-19, especially those who needed intensive care or a ventilator, are more at risk of developing pulmonary fibrosis. The scarring happens because the virus damages lung cells and triggers an exaggerated immune response. The prolonged inflammation during severe COVID-19 also contributes to the formation of scar tissue. As a result, individuals recovering from severe Covid-19 may experience ongoing breathing difficulties and reduced lung function.

To manage pulmonary fibrosis linked to Covid-19, early detection is important. Doctors use tests like imaging studies and lung function tests to identify fibrotic changes. Treatment may involve medications to reduce inflammation and fibrosis, oxygen therapy to support lung function, and rehabilitation programs to improve breathing.

The difference between Flu, a Cold and Covid-19

Influenza (flu), the common cold, and Covid-19 are all respiratory illnesses caused by different viruses, and they have some key differences.

• Flu (Influenza): Influenza viruses, primarily influenza A and B, cause the flu. Symptoms usually have a sudden onset, including fever, chills, cough, sore throat, runny or stuffy nose, muscle or body aches, fatigue, and sometimes vomiting or diarrhoea. Severe complications such as pneumonia can occur, especially in high-risk groups.
• Common Cold: Several viruses, including rhinoviruses and coronaviruses, can cause the common cold. Symptoms often develop gradually and are typically milder than the flu. They may include a runny or stuffy nose, sneezing, sore throat, cough, and mild body aches. The common cold rarely leads to serious health problems.
• Covid-19: Covid-19 is caused by SARS-CoV-2, a novel coronavirus. Symptoms can appear 2-14 days after exposure and may include fever, cough, shortness of breath, fatigue, body aches, loss of taste or smell, sore throat, and sometimes gastrointestinal symptoms. Covid-19 can lead to severe respiratory issues, pneumonia, acute respiratory distress syndrome (ARDS), and other complications.
• It’s important to note that the symptoms of these illnesses can overlap, and testing may be necessary for an accurate diagnosis, especially with the similarities between flu and Covid-19. Consulting healthcare professionals for guidance on testing, treatment, and prevention is advisable.

A covid-19 Cytokine Storm

In a Covid-19 cytokine storm, various T-helper cells and cytokines play crucial roles, contributing to an exaggerated and dysregulated immune response. Here is a list of key T-helper cells and cytokines involved, along with a brief explanation of their roles:

T-Helper Cells:

• TH1 Cells: Cytokines Produced: Interferon-gamma (IFN-γ), Tumour Necrosis Factor-alpha (TNF-α). Role in Cytokine Storm: Excessive activation can lead to intense inflammatory responses, contributing to the cytokine storm.
• TH2 Cells: Cytokines Produced: Interleukin-4 (IL-4), Interleukin-13 (IL-13). Role in Cytokine Storm: Imbalance favouring TH2 over TH1 responses may contribute to immune dysregulation and cytokine storm.
• TH3 Cells: Cytokines Produced: Regulatory T cells involved in immune tolerance. Role in Cytokine Storm: Deficiency in TH3 cell activity may contribute to a loss of immune regulation and exacerbate inflammatory responses.
• TH17 Cells: Cytokines Produced: Interleukin-17 (IL-17). Role in Cytokine Storm: Exaggerated TH17 responses may contribute to the release of pro-inflammatory cytokines, leading to widespread inflammation.

Additional T-Helper Cells:

• TH9 Cells: Cytokines Produced: Interleukin-9 (IL-9). Role in Cytokine Storm: Less studied but may contribute to cytokine storms under certain conditions.

Other Immune Cells:

• Macrophages: Cytokines Produced: Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNF-α). Role in Cytokine Storm: Activation and release of pro-inflammatory cytokines contribute to cytokine storms.
• Natural Killer (NK) Cells: Cytokines Produced: Interferon-gamma (IFN-γ) and others. Role in Cytokine Storm: Dysregulation of NK cell activity has been implicated in cytokine storm-associated diseases.

Key Cytokines:

• Interleukin-6 (IL-6): Role in Cytokine Storm: Elevated IL-6 levels are a hallmark of cytokine storms, contributing to severe inflammation and tissue damage.
• Tumour Necrosis Factor-alpha (TNF-α): Role in Cytokine Storm: Pro-inflammatory cytokine promoting inflammation and tissue damage.
• Interleukin-1 beta (IL-1β): Role in Cytokine Storm: Pro-inflammatory cytokine contributing to the cytokine storm.
• Interleukin-17 (IL-17): Role in Cytokine Storm: Produced by TH17 cells, contributes to inflammatory responses and cytokine storms.

Mechanism: The cytokine storm is triggered by the immune system’s response to the SARS-CoV-2 virus. Immune cells release large amounts of cytokines, resulting in an excessive and uncontrolled immune response.

Elevated levels of pro-inflammatory cytokines contribute to severe respiratory symptoms, widespread inflammation, and organ damage. Targeted therapies aim to modulate specific cytokines and reduce inflammation to improve outcomes in severe Covid-19 cases. Understanding the involvement of these T-helper cells and cytokines is crucial for developing targeted therapies to manage cytokine storms and associated complications in severe infections like Covid-19.

Which other viruses or conditions can cause a cytokine storm?

A cytokine storm refers to a severe and excessive immune system response characterized by the uncontrolled release of pro-inflammatory signaling molecules called cytokines. Cytokines play a crucial role in regulating the immune response and maintaining homeostasis in the body. However, when the immune system becomes dysregulated, it can lead to an overwhelming production of cytokines, resulting in a cytokine storm.

Cytokine storms can be triggered by various factors, including infectious agents such as viruses, bacteria, and fungi, as well as certain diseases and conditions. Some of the key causes include

Viral Infections:

• Influenza (Flu): Severe cases of influenza, especially influenza A, have been associated with cytokine storms. The 1918 influenza pandemic is a historical example where cytokine storms contributed to the high mortality rate.
• Coronaviruses: Certain severe cases of respiratory viruses, such as the SARS-CoV and SARS-CoV-2 (responsible for severe acute respiratory syndrome, or SARS, and Covid-19, respectively), have been linked to cytokine storms.

Bacterial Infections:

• Some bacterial infections, particularly those causing sepsis, can trigger a cytokine storm. Sepsis is a life-threatening condition where the body’s response to infection becomes dysregulated.

Autoimmune Diseases:

• Certain autoimmune disorders, such as rheumatoid arthritis and systemic lupus erythematosus (SLE), can lead to chronic inflammation and an increased risk of cytokine storms.

Immune System Disorders:

• Disorders that affect the immune system, such as hemophagocytic lymph histiocytosis (HLH), can result in an overactive immune response and cytokine storm.

Therapies and Treatments:

• Some cancer treatments, such as certain immunotherapies, can trigger a cytokine release syndrome (CRS), which shares similarities with a cytokine storm.

The cytokine storm is characterized by the release of various pro-inflammatory cytokines, including interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), and interferons. Excessive cytokine release can lead to systemic inflammation, multiple organ failure, and a range of severe symptoms.

Managing cytokine storms often involves addressing the underlying cause, such as treating the infection or managing the autoimmune condition. In some cases, anti-inflammatory medications or immunosuppressive drugs may be used to modulate the immune response and reduce the severity of the cytokine storm.

The process throughout the body when it encounters a virus or bacteria

When the body encounters a virus or bacteria, a sophisticated and coordinated process unfolds to defend against the invading pathogen. Here’s a comprehensive overview of the immune response:

• Recognition: Immune cells, such as macrophages and dendritic cells, recognize and capture the pathogens. Pathogen-associated molecular patterns (PAMPs) on the surface of the invaders are detected.
• Innate Immune Response: The innate immune system is activated, leading to the release of chemical signals like interferons and cytokines. Phagocytes, such as neutrophils and macrophages, engulf and neutralize pathogens.
• Adaptive Immune Response Initiation: Antigen-presenting cells (APCs) present pathogen fragments (antigens) to T cells, initiating the adaptive immune response.
• B Cell Activation: B cells are activated and differentiate into plasma cells, producing antibodies specific to the pathogen.
• Antibody Binding: Antibodies bind to the surface of the pathogen, neutralizing it or marking it for destruction.
• T Cell Activation: Helper T cells activate cytotoxic T cells, which directly attack infected cells. Regulatory T cells modulate the immune response to prevent excessive inflammation.
• Cellular Immunity: Cytotoxic T cells recognize and eliminate infected cells. Memory T cells are generated for long-term immunity.
• Complement System Activation: The complement system is activated, enhancing the immune response through various mechanisms.
• Inflammation: Inflammatory responses, including increased blood flow and recruitment of immune cells, help contain and eliminate pathogens.
• Fever Response: Elevated body temperature inhibits pathogen replication and enhances immune function.
• Resolution and Tissue Repair: Pathogens are cleared, and damaged tissues undergo repair. Anti-inflammatory signals help resolve the immune response.
• Memory Formation: Memory B and T cells are generated, providing long-term immunity against the specific pathogen.

Throughout this process, communication between immune cells, the release of signaling molecules, and the execution of specific immune functions contribute to the body’s defense. The immune response is a dynamic and adaptable system that adapts to various pathogens, ensuring protection and maintaining overall health.