Viral Fusion Inhibitor

Viruses cannot reproduce by themselves.  They must first attach to a human host cell, where they hijack the cell’s reproductive capabilities to replicate.

ViraFend® inhibits the attachment (fusion) of viruses to host cells, and supports the body’s immune system’s ability to regulate virus replication.*

Activated Humic Acid

ViraFend’s active ingredient – Activated Humic Acid – has been shown to help regulate viral replication.  Humic Acid displays an  ability to bind to, or ‘coat’ a wide range of viruses.  This inhibits viruses from attaching to human host cells – the necessary first step in the virus life cycle that enables viruses to reproduce inside the body.*

Research and Testing

Numerous clinical studies, in vivo and in vitro have confirmed the efficacy of ViraFend’s Humic Acid activity against viral attachment for a wide range of viruses.  Significant reductions in viral loads were demonstrated against Herpes viruses, Influenza (flu) viruses, and the Shingles virus (Herpes zoster).*

"With most viruses, the inhibitory effect of Humic Acid is directed against an early state of virus replication, virus attachment to cells."

Prof. Renate Klocking, PhD
Institute for Anitviral Chemotherapy

VIRAFEND® VIRUS DEFENSE FORMULA PRODUCTS

ViraFend Virus Defense Formula is available in formulations for Cold Sore & Herpes Viruses, Influenza (Flu) Viruses, and the Shingles Virus. Click any of the images below to view each product's full website.

ViraFend®
Virus Defense Formula

COLD SORE & HERPES VIRUSES

ViraFend®
Virus Defense Formula

FLU VIRUSES

ViraFend®
Virus Defense Formula

SHINGLES VIRUS

VIRAFEND® SCIENCE

The Science Behind ViraFend®

To understand the potential of ViraFend, and its primary active ingredient – Activated Humic Acid – it is first important to understand how viruses reproduce.

Although viruses do have genes, they do not have a cellular structure, which is the basic unit of life.  Viruses also do not have their own metabolism, and require attachment to a host cell to make new viruses.

This is an extremely important point: viruses cannot reproduce by themselves.  They must attach to a host cell, insert their viral DNA or RNA, and use the host cell’s reproductive mechanisms to act as an incubator.  Viral DNA and RNA ‘trick’ or co-opt the host cell into reproducing the virus.

If a viral particle cannot attach to a host cell in the first place, it cannot insert its viral DNA or RNA, and thus it cannot reproduce.  Viruses that cannot attach to host cells are thus more vulnerable to the human immune system, which can then act more effectively to eliminate the attacking virus.

The process of a virus attaching to a host cell, so it can insert its DNA or RNA into the host cell is called ‘Viral Fusion’, or ‘Virus Attachment’.

Interfering with the ability of a virus to attach to a host cell, so it is not able to reproduce is referred to as ‘Viral Fusion Inhibition’ – one of the leading topics in viral therapeutics.  Viral Fusion Inhibition (or Virus Attachment Inhibition) refers to the ability of a substance to interfere with and thus inhibit the ability of the virus to complete attachment to its target host cell.

The Virus Life Cycle

The Virus Life Cycle is comprised of 6 stages – this is true for virtually every virus that affects humans.  ViraFend targets the first stage – Virus Attachment, to inhibit the ability of a virus particle to attach to a human host cell. If the virus cannot attach, it cannot insert its DNA or RNA into the host cell, and thus cannot replicate.

Clinical studies show that the poly-ionic Humic Acid occupies positively charged domains of the viral envelope glycoproteins, which are necessary for virus attachment to the cell surface (Nyets, et al.)

Cold Sores and Herpes Viruses

Often referred to by the more socially acceptable terms ‘Cold Sores’, or ‘Fever Blisters’, the eruptions that occur in and around the oral / facial area are the result of the action of the Herpes Simplex Virus Type 1 (HSV-1).  As the HSV-1 virus is transmitted through direct contact, kissing and sexual activity (and primarily through ‘viral shedding’), for decades, ‘having Herpes’ was considered a sign of promiscuous sexual behavior, and more socially friendly terms, like ‘Cold Sores’, were coined.

But the facts are that ‘Cold Sores’ and ‘Fever Blisters’ are indeed outbreaks caused by the Herpes virus.  In fact, the Herpes virus is in reality primarily transmitted as much by ‘Viral Shedding’ as it is by direct sexual contact.  Almost half of people infected with the Herpes virus don’t even know it, as they may never have experienced a visible outbreak, or didn’t know that certain symptoms were those of Herpes. If you’ve ever had a cold sore, you have the HSV-1 virus in your system.

Flu (Influenza) Viruses

Influenza, commonly known as the “flu,” is an extremely contagious respiratory illness caused by caused by one of the influenza viruses, most commonly influenza type A or type B viruses.  Flu appears most frequently in winter and early spring.

While more than 100 different viruses can cause a cold, only influenza virus types A, B, and C cause the flu.

Learn what your body’s immune system does and how to strengthen it so you can boost your odds of staying well.

Type A, B and C Flu Viruses

There are three types of flu viruses: A, B, and C.  Type A and B cause the annual influenza epidemics that have up to 20% of the population sniffling, aching, coughing, and running fevers.  Type C also causes flu, but the symptoms are much less severe.

Usually, the virus is spread through the air from coughs or sneezes. This is believed to occur mostly over relatively short distances.  It can also be spread by touching surfaces contaminated by the virus and then touching the mouth or eyes. A person may be infectious to others both before and during the time they are showing symptoms.

Influenza spreads around the world in a yearly outbreak, resulting in about three to five million cases of severe illness and about 250,000 to 500,000 deaths.

  • Fever and extreme coldness (chills shivering, shaking (rigor))
  • Cough
  • Nasal congestion
  • Vomiting
  • Runny nose
  • Sneezing
  • Body aches, especially joints and throat
  • Fatigue
  • Headache
  • Irritated, watering eyes
  • Reddened eyes, skin (especially face), mouth, throat and nose

Viruses can replicate only in living cells.  Influenza infection and replication is a multi-step process: First, the virus has to bind to and enter the cell, then deliver its genome to a site where it can produce new copies of viral proteins and RNA, assemble these components into new viral particles, and, last, exit the host cell.

When an infected person sneezes or coughs, more than half a million virus particles can be spread to those close by.   In otherwise healthy adults, influenza virus shedding (the time during which a person might be infectious to another person) increases sharply one-half to one day after infection, peaks on day 2 and persists for an average total duration of 5 days – but can persist as long as 9 days.  In those who develop symptoms from experimental infection (only 67% of healthy experimentally infected individuals), symptoms and viral shedding show a similar pattern, but with viral shedding preceding illness by one day.   Children are much more infectious than adults and shed virus from just before they develop symptoms until two weeks after infection.  In immunocompromised people, viral shedding can continue for longer than two weeks.

Influenza can be spread in three main ways: by direct transmission (when an infected person sneezes mucus directly into the eyes, nose or mouth of another person); the airborne route (when someone inhales the aerosols produced by an infected person coughing, sneezing or spitting) and through hand-to-eye, hand-to-nose, or hand-to-mouth transmission, either from contaminated surfaces or from direct personal contact such as a handshake.

As the influenza virus can persist outside of the body, it can also be transmitted by contaminated surfaces such as banknotes, doorknobs, light switches, towels, and other household items.

  • Adults over 65
  • Babies or young children
  • Pregnant women
  • Individuals with heart or cardiovascular disease
  • Those with chest problems, such as asthma or bronchitis
  • Individuals with kidney disease
  • People with diabetes
  • People taking steroids
  • Individuals undergoing treatment for cancer
  • Those with longstanding diseases that reduce immune system function

The Shingles Virus

Shingles is caused by the Varicella-Zoster virus — the same virus that causes chickenpox.  After you’ve had chickenpox, the virus lies inactive in nerve tissue near your spinal cord and brain.  Years later, the virus may reactivate as shingles.

Shingles is a painful skin rash which usually appears in a band, a strip, or a small area on one side of the face or body.  It is also called Herpes Zoster, as it is a member of a group of viruses called Herpes viruses, which includes the viruses that cause cold sores and genital herpes – but the virus that causes chickenpox and shingles is not the same virus responsible for cold sores or genital herpes, which are sexually transmitted infections.

Shingles is most common in older adults and people who have weak immune systems because of stress, injury, certain medicines, or other reasons.  Half of the US population is projected to experience shingles in their lifetime.

Painful and debilitating, shingles, also poses a threat to the survival of patients who suffer from a reactivation of the chickenpox virus. They are more at risk of cardiovascular disorders, including stroke and heart attacks, which can potentially be fatal, according to a study published in the Journal of the American College of Cardiology.

A 10-year study in Asia of 23,000 people compared the risks associated with shingles between people who did and did not suffer from reactivation of the chickenpox virus.  The study showed that patients who suffered from shingles were 41% more likely to suffer a cardiovascular event.  The likelihood of developing such complications is particularly high in the year following reactivation.  Stroke and myocardial infarction occur more often after a herpes zoster that in its absence; the risk is, respectively, 35% and 59% higher.

What Causes Shingles?

Shingles occurs when the virus that causes chickenpox starts up again in your body.  After you recover from chickenpox, the virus “sleeps” (remains dormant) in your nerve roots.  In some people, it can stay dormant forever.  In others, the virus “wakes up” when disease, stress, or aging weakens the immune system.  Some medicines may also trigger the virus to reactivate and cause a shingles rash.  It is not clear why this happens.

Anyone who has had chickenpox can get shingles. You have a greater chance of getting shingles if you are older than 50 or if you have a weak immune system.

The signs and symptoms of shingles usually affect only a small section of one side of your body. These signs and symptoms may include:

  • Pain, burning, numbness or tingling
  • Sensitivity to touch
  • A red rash that begins a few days after the pain
  • Fluid-filled blisters that break open and crust over
  • Itching

Some people also experience:

  • Fever
  • Headache
  • Sensitivity to light
  • Fatigue

Complications from shingles can include:

  • Postherpetic neuralgia. For some people, shingles pain continues long after the blisters have cleared.  This condition is known as postherpetic neuralgia, and it occurs when damaged nerve fibers send confused and exaggerated messages of pain from your skin to your brain.
  • Vision loss.  Shingles in or around an eye (ophthalmic shingles) can cause painful eye infections that may result in vision loss.
  • Neurological problems.  Depending on which nerves are affected, shingles can cause an inflammation of the brain (encephalitis), facial paralysis, or hearing or balance problems.
  • Skin infections.  If shingles blisters aren’t properly treated, bacterial skin infections may develop.

Inhibiting Virus Attachment Helps Regulate Virus Replication

Herpes viruses are extremely common with more than 100 varieties having been identified in a variety of animal species, including at least 8 variations that affect humans.  All of the Herpes viruses are members of one family, the Herpesviridae, and have specific common characteristics, such as the ability to establish latency during a primary (first) exposure and infection.

This means that following initial infection the Herpes virus may lie dormant for periods of time.  It resides (or ‘hides’) within the nervous system and other cells in the body as protection from the antibodies produced by the immune system.

When inactive (dormant or latent) the virus inhabits the cell in the latent stage and does not replicate or travel throughout the body. When stimulated by factors (triggers) such as stress, illness, poor nutrition, excessive activity and even sunlight coupled with a weakened immune system, the Herpes virus re-awakens and travels through and around nerve pathways to the site of the outbreak.

The Herpes virus remains in a latent stage that can last for weeks, months or even years, and various approaches can help reduce viral load, shorten the duration and severity of outbreaks, and potentially reduce the frequency of outbreaks.

Viruses are sub-cellular organisms, extremely small in size (approximately 1/100th the size of the average bacterium), and are vulnerable the immune system when not attached to a host cell.

The Herpes virus’ most essential objective is to take over control of the host cell DNA and use it to make copies of its own DNA (or in some viruses like HIV the genetic material may be RNA which is slightly different), replicating wildly, and then releasing newly formed virus particles into the system, spreading to and attaching to new host cells, where the process repeats itself over and over.

In simple terms, virus particles that escape (are released) into the blood stream or intracellular fluids) may be identified and killed, but those which stay inside host cells replicating, or lie dormant in nerve roots between outbreaks are not.

ViraFend’s primary ingredient has been shown to be a potent Virus Attachment Inhibitor, and acts to impede the ability of viruses to attach to human host cells.

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*These statements have not been evaluated by the Food & Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease. Always seek professional medical attention for any medical concerns you may have. If this is an emergency, call 911 or go to your nearest emergency room. The information on this website is not intended as medical advice or to replace the advice of a qualified medical professional.