Thanks for your points,
@hinterland.
Firstly, in the Staphypan trial the vaccine was injected subcutaneously in gradually increasing dosages.
The patients received weekly subcutaneous injections in increasing dosages of the vaccine during the initial 8-10 week period, and thereafter once a month.
In the
instructions for the Russian Staphylococcus vaccine manufactured by
Medgamal (Медгамал) in Moscow, they also say that the vaccine must be administered in gradually increasing dosages:
A full course of treatment includes 7 injections administered once every 2 days, with the following increasing doses: 0.1 - 0.3 - 0.5 - 0.7 - 0.9 - 1.2 - 1.5 ml.
If I try out the Russian vaccine, I will start with even smaller doses initially, say 0.025 ml or even less, in order to minimize any adverse effects, should they arise. And rather than take the Russian vaccine every two days as its instructions state, I will space out these doses more, taking one dose say every week.
Secondly, it is not clear that any of the suggested alternative products contain the same or equivalent biological materials, or what mix of the components in the Staphypan vaccine is responsible for it's therapeutic effect in CFS. The Staphypan vaccine includes both coagulase positive and negative strains of staphylococci along with a toxoid.
It certainly is a gamble trying the Russian vaccine, and it may not work at all, for the reasons you give.
The main components of the Staphypan® vaccine are:
Alpha toxin
Enterotoxin A
Enterotoxin B
Toxic shock syndrome toxin 1 (TSST-1)
Cell wall antigens
Lipase
Table 2 of the Olaf Zachrisson 2004 Study
These ingredients were determined by Zachrisson et al, 2004. See:
Immune modulation with a staphylococcal preparation in fibromyalgia/chronic fatigue syndrome: relation between antibody levels and clinical improve.
Full paper
here.
Enterotoxin B seems to have significant connection to autoimmune disease:
Possible Role of Staphylococcal Enterotoxin B in the Pathogenesis of Autoimmune Diseases
Enterotoxin B plays a critical role in the pathogenesis of autoimmune disorders either by initiating the autoimmune process or by inducing a relapse in an individual in clinical remission from an autoimmune disorder. Enterotoxin B can directly activate T lymphocytes, leading to the release of cytokines, superoxides, or other mediators of inflammation either directly or indirectly, because of its unique ability to cross-link human major histocompatibility complex (MHC) class II and T cell receptors (TCR), forming a trimolecular complex.
So in terms of the mechanism behind the major improvements in ME/CFS provided by Staphypan®, enterotoxin B may play the central role, if we consider ME/CFS as an autoimmune condition.
The way enterotoxin B modulates autoimmunity may involve its effects on the CD28 receptor.
It has recently been discovered that enterotoxin B binds to the CD28 receptor (refs:
here and
here), and this receptor has been linked to autoimmune disease (CD28 controls differentiation of regulatory T-cells, which play a central role in maintaining immune self-tolerance).
Interestingly enough, the CD28 receptor super-agonist drug TGN1412 is being tested as a treatment for autoimmune diseases. But TGN1412 was also the drug in the 2006 Northwick Park Hospital London clinical trial disaster, in which several young men became very ill with organ failure. So activating the CD28 too much can be very dangerous. After this clinical trial disaster, this TGN1412 drug is now making a
comeback, using doses 10 to 20 times less (and being renamed as TAB08).
As for Staphylococcus
enterotoxin A, this had two distinct binding sites for major histocompatibility complex (MHC) class II molecules (ref:
here).
