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HERPES SIMPLEX VIRUS


Background:

Although clinical trials have never been carried out specifically for HSV patients, the enormous amount of patient feedback regarding the sudden disappearance of HSV symptoms, begged the question, "why was this happening and how". Referencing the various clinical studies on file, gave us the answer. To understand the mechanism of action, one first needs to understand how the herpes virus affects the immune system.

What is Herpes Simplex?

Herpes is usually referred to the sexually transmitted herpes simplex virus (HSV) type 2. This virus is closely related to herpes simplex virus type 1, which is the cause of common non sexually transmitted cold sores. These two viruses are among the eight members of the herpes virus family that infect humans and cause a variety of illnesses such as cold sores, brain infection (encephalitis), chickenpox (herpes zoster), various cancers and up to 70% of the cases of Bell's palsy (facial paralysis)

The primary difference between the two infections is the principal site of infection—mucous membranes of the lips and nearby oro-facial skin for HSV-1, and the genital skin for HSV-2. After initial infection, these viruses both travel to sensory nerves, where they reside as life-long, latent viruses. When the viruses reactivate to cause symptomatic disease, they travel back to the respective skin areas served by these nerves, leading to the different (oral vs. genital) distributions of cold sores.

Pharmaceutical drug protocol

Unfortunately doctors still insist on the symptomatic approach and can prescribe any one of the following drugs: aciclovir (Zovirax), valaciclovir (Valtrex), famciclovir (Famvir), and penciclovir. Docosanol (Abreva) was approved by the FDA in July 2000. In March, 2007 it was the subject of a United States class-action suit against Avanir and GlaxoSmithKline as their claims about halving recovery times, were false.

The Qina approach

The herpes virus is able to suppress expression of pro inflammatory cytokines which are produced by macrophages, by decreasing the stability of mRNAs, thereby potentially impeding the antiviral host response to infection. Scientific findings have establish that Macrophages are important components of defence against HSV through their production of antiviral molecules Tumour Necrosis Factor, Nitric Oxide, and Interferon.

Although, macrophages are the important line of defence against HSV they are vulnerable to high viral loads which decreases their normal activity and inhibits their nitric oxide production and causes cell mortality.

Conclusion:

Qina has been proven to activate macrophage activity resulting in it's modulation, of the various components of the immune response that is responsible for the stimuli of anti viral molecules of which Nitric Oxide is one. The suppression of macrophages by the HSV, reduces it's ability to release NO, resulting in unimpeded viral reactivation.

There is no cure for herpes to date. Supporting your immune system should be your first goal as a weakened immune system is more prone to outbreaks.


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References

  1. Journal of General Virology, Vol 79, 2785-2793
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  3. The Journal of Immunology, 1999, 162: 2895-2905.
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  7. Journal of General Virology, Vol 79, 2785-2793.
  8. J Clin Invest. 1993 June; 91(6): 2446–2452.
  9. The Journal of Immunology, 2001, 167: 2202–2208.