UNDERSTANDING THE HERPES VIRUS

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Why cold sores, also called fever blisters, may be difficult to treat. 

Cold sores are caused by a herpes simplex virus, or HSV. Herpes viruses owe their ability to spread by evading the host immune system, while surviving and replicating within the host cells. The herpes virus develops a protective outer envelope when it infects the host. The enveloped virus first binds to, and then enters cells in the body. After viral entry, the virus replicates rapidly inside the host’s cell. The greatly expanded number of viral particles are then released from the cell to spread to other cells, repeating the replication process.  

The cold sore early stage typically begins with a tingling sensation on the lip. Within 12- 24 hours the early sore, a red bump, develops.  It then may take 1-2-3 days to form a blister(s), i.e., the cold sore. The sore may build up and then excrete a highly infectious clear/yellow liquid, the so-called “weeping phase.” The final phase is the formation of a scab, which can take 7+ days to resolve, and up to several weeks in the immune compromised individual.  

Both the blister, and the subsequent scab that forms, can develop a microscopic biofilm that protects the virus from the exposed environment. The protective viral envelope and biofilm each challenge the body’s immune system to fight the virus and can also hinder certain treatments. 

Why cold sore treatments have limited effectiveness.

Most cold sore treatments do not directly affect the virus, but focus mainly on relieving the symptoms, namely itch, tingling and pain, where the effects are typically of temporary nature. The immune system is left to deal with the virus on its own, where the lesions and subsequent scab typically last anywhere from 7-14 days, and up to 3-4 weeks in some cases, especially in an individual with a compromised immune system. Other treatment options may have some direct viral effects, but they have limitations. 

Mechanism of action and what it means? 

Combining the information from our lab studies and existing publications, it is  hypothesized that a key mechanism of action for Zap-H™ is the ability of its ingredients to disrupt the protective viral envelope (see “The Zap-H™ Benefit" below for more details). Once the viral envelope is disrupted, it exposes the virus‘ internal components to the body's immune system. This allows the immune system to more effectively deal with healing the virus because the viral particle's ability to propagate has been greatly diminished. Also, the body‘s immune system can then identify critical pieces of the virus itself that have been exposed. This further helps the immune system to learn how to build protective measures against the virus. These learned protective measures help the body to prevent the frequency and severity of any potential future outbreaks.

What's a viral envelope and why do I care? 

The viral envelope (also called viral membrane) protects the HSV viral DNA.  Disrupting the viral envelope can lead to either direct killing of the virus by Zap-H™ or it can allow for the immune system to target and kill the HSV viral particles.  It is well established that numerous fatty acids kill numerous viruses and this is accomplised by disrupting their viral envelopes, or membranes.  Zap-H™ comprises such fatty acids that disrupt viral membranes.  Furthermore, in-vitro (i.e., lab tests) testing with Zap-H™ has shown rapid killing of viral particles.  In this way, Zap-H™ kills HSV viral particles by disrupting theinr envelopes.  

Thormar H, et al; Inactivation of enveloped viruses and killing of cells by fatty acids and monoglycerides. Antimicrob Agents Chemother. 1987;31(1):27-31. doi:10.1128/AAC.31.1.27. 

Further yet, although numerous fatty acids/ oils can kill viruses, the combination of ingredients in Zap-H™signficanlty enhances, i.e., synergizes, such viral killing.  In this way, the combination of Zap-H™ ingredients is profoudly more effeftive than using such fatty acids/ oils alone.  Further yet, when an antiviral formulation is applied topically, it needs to penetrate into the skin such that the active ingtredients can actually reach the viral particles which are buried under the skin, and potentialy within bioflm.  Zap-H™ ingredients comprise a water-based formulation which has rapid skin penetration, and this enhances its clinical efficacy (i.e.., the active ingredients can actually reach, make contact with the viral particles).  Further yet, a formulation that absorbs weill does not leave a visible or irritating residue on the skin/ lip.  

Our the hospital clinical study, and other clinical test results confirm this as that the combination of ingredients in Zap-H™ improves the antiviral features beyond using any of the ingredients alone. 

Zap-H™ has also shown antiviral efficacy agsints other viruses that were tested in the lab.  These pertain not only to herpesvirus, but also coronavirus, RSV (respiratory syncytial virus), influenza and Mpox viruses.  The formulations are altered for specific viruses for best results.   The same formula is not optimal for every virus.  We do not advocate that the Zap-H™ formulation should be used to mitigate symptoms for these other viruses, but they further confirm the antiviral features of Zap-H™ ingredients.  

Why the Herpes Virus is difficult to treat.

The herpes HSV-1 virus is the main cause of cold sores/fever blisters on lips. A similar herpesvirus, HSV2, is the main cause of genital herpes, but either one of these 2 versions can cause oral cold sores. Herpes viruses owe their successful spread to their complexity, which has enabled them to effectively slow down the human immune system in several different ways. Glycoproteins of the herpesvirus envelope play a significant role in the early interactions, attachment, and entry of viral particles into the host cell. They modulate the immune system to maintain a presence in the infected host. They maintain a balance between preventing being killed by the immune system, and preventing host cell death, as their survival depends on host cell survival. Herpesvirus has evolved a mechanism to remain dormant in the body for long periods of time, wherein they linger in a hibernation state known as viral latency. 

Herpes Virus Replication

The herpes virus is classified as a DNA virus and an enveloped virus. Viral DNA is stabilized by a shell of proteins called the capsid. Together the DNA and capsid are referred to as the nucleocapsid. The nucleocapsid is surrounded by the outer envelope. The outer envelope is formed from the host cell membrane. 

The virus is always surrounded by this envelope except after it enters a cell, whereby the nuclear material, nucleocapsid, is released. The released nucleocapsid enters the host nucleus, wherein lies the host’s DNA. In the nucleus the viral particles replicate. After subsequent release from the nucleus, the newly formed nucleocapsid particles fuse with the host cell‘s outer membrane, whereby they acquire a part of the host membrane, becoming the viral envelope for all the newly formed herpes viral particles. The enveloped viral particles are released by exocytosis, which is also referred to as a budding mechanism, with subsequent spread to other cells. 

The herpes viral particles have a predilection for neurons near the base of the brain, in an area called the trigeminal ganglion. The virus lies dormant within these nerve cells and can do so for months to many years, even 30 or more. It can be activated by numerous factors, and this may vary between individuals. Triggering factors include stress, lack of sleep, exposure to sun, cold wind, a cold, flu or other illness, a weak immune system, and changing hormone levels. 

The Zap-H™ Benefit

Zap-H™ consists of ingredients that together result in synergistic viral envelope and biofilm disrupting effects that are not possible with any single compound acting alone. Plant oils have long been known to have antiviral properties.  Fatty acids/ oils have effects against bacteria, such as Staphylococcus aureus, that can cause disease. However, it does not kill beneficial bacteria, such as Bifidobacteria and Lactobacilli.  Fatty acids are also known to have biofilm disrupting effects against numerous bacteria. Fatty acidfs can reduce inflammation in epithelial cells, such as those lining the mammary glands. Excess inflammation contributes to pathogenic bacterial growth. The anti-inflammatory feature helps to heal the scab, which is a form of a wound.  

Nuerous fatty acids have known antiviral properties. Their mechanis of action is that they break down a virus’ envelope, a form of membrane, which results in the killing of the viral particle. 

While laboratory studies show viral envelope distuption and a viral killing feature by fatty acids, any clinical effect has not been evaluated by the FDA.  However, the rapid in-vitro viral envelope disruption correlates with a rapid in-vivo effect (i.e. demonstrated with a double-blind, hospital clinical study showing a significant reduction in time for symptoms to disappear).  in other words, both our lab tests and reseach in the past correlate highly with results obtained with clinical use of Zap-H™.  

Our clinical experience further shows that individuals using Zap-H™ anecdotally note that it is effective even if treatment application begins after the blisters have formed, i.e., at 5 days after onset of a cold sore (see also below on biofilm).   This is a benefit over docosanol based products and prescription antiviral medications, which need to be started within 2 days of the onset of a cold sore, being ineffective once blisters form.  

Zap-H ™ & Biofilm

An additional benefit for Zap-H ™ pertains to biofilm. Biofilm is a complex extracellular matrix that is formed by microorganisms which protects them from substances in their local micro-environment, and this includes antibiotics, antiviral agents, and some antiseptic agents.  

Zap-H ™ cream was initially developed as an antibacterial biofilm disrupting technology, before it was found to have antiviral properties. The blend of Zap-H™ ingredients breaks down biofilm in multiple types of microorganisms. In-vitro lab testing at a top microbiology testing center demonstrates effects against mature biofilm organisms, and this includes Gram positive Staph. aureus and Enterococcus; Gram negative Pseudomonas aeruginosa, E. coli, and Klebsiella pneumonia; and Candida fungal biofilm. 

When open sores develop, bacteria infiltrate such open wounds, and form biofilm as a manner by which to protect themselves. Bacteria are known to reside within biofilm in the eschar (i.e., scab) above a wound bed, such as a scabbed cold sore lesion. Viruses are known to lodge within bacterial and fungal biofilms. In this respect, after a cold sore blister breaks and the scab forms the herpes virus can exist in the bacterial biofilm of the cold sore eschar. Because Zap-H™ disrupts biofilm, this is yet an additional benefit as it can target viruses that may be present within biofilm located on open sores. Moreover, if one could breakdown biofilm (such as with Zap-H™), it would expose the encased viral particles, rendering them susceptible to topical viral envelope-disrupting agents, such as Zap-H™, and the body's immune response. In other words, Zap-H™ does both – it first disrupts the biofilm to expose the viral particles, and subsequently dissolves the viral membranes thus allowing for the killing of the now-exposed viral particles by the immune system. This is correlated clinically by individuals, where treatment of cold sores with Zap-H™ was started up to 5 days from symptom onset. At this stage the outbreak formed an eschar (i.e., scab). Nonetheless, subjects reported that their symptoms were resolved more quickly with Zap-H™ application, even at this relatively late stage in treatments, as compared to an untreated cold sore scabbed lesion.  

Zap-H™ & Skin Absorption

A yet additional benefit for Zap-H™ is rapid skin absorption. When we tested numerous over-the-counter (OTC) products, it was noted that most did not have good skin absorption properties. Docosanol, for example, has shown poor skin permeation properties. In fact, the Product Monograph from a pharmaceutical company, the manufacturer/ distributor of a docosanol 10% cream, on November 26, 2013, specifically states “Dermal and gastrointestinal absorption of docosanol ..... is limited…...”.  

If a composition does not absorb through the skin, then one can imagine that there is limited ability for such a product to target a virus, which is lodged deep underneath the skin surface.  Zap-H™, on the other hand, absorbs quickly, typically within 5-10 minutes. This is due to the presence of skin permeation enhancers in the Zap-H™ formula. Such rapid penetration through the skin and into the local tissues allows for the ingredients to reach the cells. Any viral particles that are either ready to enter a host cell, or those newly formed viral particles that have exited the cells can be targeted by the absorbed Zap-H™, which will disrupt the viral envelope, allowing the immune system to eradicate the virus. 

Genital Herpes

The genital herpesvirus (HSV2) is structurally very similar to the cold sore HSV1 virus particle. The viral envelopes are similar, as both are formed from the host cell wall. In this respect, because Zap-H™ targets the viral envelope, it theoretically would have effectiveness against the genital HSV2 viral envelope. (Clinical testing for genital herpes has not yet been performed.)  At this time we are not able to recommend Zap-H™ for use on HSV2 or genital herpes sores.  The information herein is provided for healthcare professionals. 

Shingles

Shingles rash is the reactivation of the chicken pox herpes virus (Varicella Zoster, or Herpes Zoster - HZ) infection in adults.  It can be very painful and debilitating.  Zap-H™ has not been formally tested for shingles, however, because shingles is caused by a similar herpes virus, with a similar viral envelope, anecdotal reports indicate that it may be effective in relieving pain symptoms of the shingles rash.  Because no formal testing has been done for shingles, at this time we cannot recommend the use of Zap-H™ for applicatoin on shingles sores. This information is provided for healthcare professionals. 

PHOTO:  Day 6, after applying Zap-H™ on Day 4, 5 and 6.  Painful symptoms were relieved more rapdily than the typical  duration of 3-5 weeks. 

Note. This is only one example, and it does not prove that Zap-H™ will have similar results for other subjects. We show this to highlight that Zap-H™ ingredients have a unique ability to potentially help the body's immune system to better deal with a viral skin infection. Zap-H™ does not cure any disease and has not been tested or approved by the FDA for use in treating symptoms associated with a shingles outbreak. This information is provided for healthcare professionals.