Summary of contents
A preliminary account of the topical application of blood to shingles lesions. A mode of action suggested. Some support for the suggested mode of action outlined.
The shingles blood cure practice
The cure is widely practiced in Ireland, particularly in rural areas. To effect the cure drops of blood are drawn from the finger of the curer by pricking the finger with a pin. The blood is immediately smeared from the finger onto all visible shingles lesions (in any stage of development) of the person suffering the infection and is then left to dry. No other ointment, cream or dressing is applied except the blood. Persons treated in this fashion generally report that the spread of the infection is immediately halted, that dramatic relief from pain occurs within 24hrs and complete cure is accomplished within days.
Sometimes the blood application procedure is repeated on successive days but often the application is made only once. The procedure takes only so long as is required to cover the entire affected area with blood. It appears to be effective even with cancer patients. Many of the 'curers' are famous in their localities for the cure and even go into hospitals in a 'clandestine' fashion to apply the 'cure' having been invited by relatives with long-term shingles. Most curers are convinced that the cure is 'in the blood'.
Mode of Action
The following is a proposed mode of action for the above.
Upon application of the blood to a shingles lesion (Fig. 1) T-Lymphocytes from the donor come into contact with viral antigen (Zoster) on the skin surface of the patient (Fig.2). The antigen stimulates the donor's lymphocytes to produce soluble lymphokines (e.g. interleukin, interferon or transfer factor) which are absorbed by the recipient (Fig.3).
The absorbed lymphokines in turn stimulate and 'kick-start' the recipients own dysfunctional T-lymphocytes [2,3] and/or macrophages to attack the virus and virally-infected keratinocytes thus initiating recovery (fig.4.).
These lymphocytes and macrophages, now properly stimulated and activated, secrete further soluble mediators which in turn activate others so that recovery continues. Since a considerable inflammatory process occurs in shingles it is possible that only a small amount of the 'right' soluble stimulatory factor needs to be absorbed to act as a 'kick-start' for the patient's macrophages/lymphocytes/NK cells already present at the site. Recovery continues once the kick-start has been given. On the other hand it may be that a number of mediators are secreted and absorbed and together they produce the therapeutic effect. That it is possible for some factor to be absorbed is without doubt. The chemical acyclovir is used as a topical treatment for shingles (in the form of Zovirax cream) and topical corticosteroids are used in the treatment of psoriasis. Immune response modifiers are also used topically and have FDA approval [7,8,9].It is also well known that traumatized skin is many times more absorbing that the intact membrane.
Possible alternative (or concurrent) mode of action
A possible alternative immunological explanation involves the keratinocytes themselves. These are now known to secrete many soluble immune system mediators particularly of the interleukin family (under a variety of stimulants[1]). It may be possible that these mediators or other compounds of the blood (perhaps as yet unknown) or even the formed elements themselves stimulate the keratinocytes to secrete the mediator(s) required to enhance the local immune response and therefore alleviate the condition.
Other relevant and interesting points (a) One curer who found that he could not cure the condition after having two hip replacements and has discontinued 'practising'. (b) A success rate approaching 100% according to preliminary investigation (where success means halting further spread of the infection, dramatically relieving pain and curing the condition completely within 7-10days). (c) The extent of the practice, which is far more widespread than is generally known. Most GPs in Ireland are aware of the practice (some have been cured themselves in this manner not having responded to the normal drug therapy i.e. acyclovir) but none appear to know the extent of its practice. I estimate that there are approx. 80 persons in Ireland 'practising' this cure on a weekly/monthly basis. (d) Despite coming into intimate contact with fresh shingles lesion on a regular basis the curers themselves remain unaffected. Factors suggesting and supporting the proposed mode of action (a) Shingles infection is considered to be a cell-mediated immune system dysfunction. The use of antibody as a therapy does not cure the condition but does alleviate the severity of attack. Hence a 'cellular' mode of action is the most likely. (b) Many scientific trials and reports support an immunological explanation. In one report the transfusion of white cells and injection of transfer factor to patients are described as dramatically beneficial [4]. In another interferon is shown to appear in the vesicle fluid of recovering patients and treatment with interferon diminishes virus dissemination in patients with Hodgkin's disease [5]. Transfer factor seems to accelerate cessation of vesicle formation and initiation of crust formation and to increase serum interferon concentration [6]. Such experimental results lend credence to an immunological explanation despite the existence of a considerable placebo effect in trials. (c) Several aspects of the 'phenomenon' suggest and support an immunological explanation rather than a psychosomatic one. These include the curer whose blood no longer 'worked' after having hip replacement, the near 100% success rate of the cure and that fact that practising curers themselves do not contract the infection despite continuous and close contact with it. References [1] 'IL-12 is expressed and released by Human Keratinocytes and Epidermoid Carcinoma Cell lines'; Journal of Immunology; Dec 15, 1994. 5366-5371. [2] 'Herpes Zoster and Impaired Cell-Associated Immunity of the Varicella-Zoster Virus in Patients with Hodgkin's Disease'; Amer. J. of Med. Jan 1977;62(77-85). [3] 'Cell-Mediated immunity to Varicella-Zoster Antigen in Acute Herpes Zoster (Shingles)'; Clin.Exp.Immunology. (1972) 14,181-185. [4] 'Varicella-Herpes Zoster Virus'; Thomas H.Weller, Chap 23, pg 588. [5] 'The Human Herpes Viruses'; J.A.Zaia, pg17. [6] 'Textbook of Human Virology'; Chap 30, pg 846, Schauf and Tolpin. [7] 'ALDARA (imiquimod) Cream, Dermatologic Use'; [8] 'Topical immunotherapy in dermatology'; [9] 'Topical Tacrolimus: A New Therapy for Atopic Dermatitis';
