This invention is a method of killing the stealthy intra-cellular 
bacteria which are key to the 
pathogenesis of both Acquired 
Immune Deficiency Syndrome(s) (AIDS) and Cancers. It is currently believed that the 
disease(s) known as AIDS are caused by a 
virus, the 
Human Immunodeficiency Virus (HIV). But much of the long-term (chronic) destruction of the 
immune system in AIDS is actually caused by tiny, stealthy, antibiotic-
resistant bacteria. The HIV 
virus weakens the 
immune system so that the stealthy 
bacteria can proliferate out-of-control, and the damage of AIDS is done just as much by these 
bacteria as by any 
virus. These very tiny L-form 
Cell-Wall-Deficient (CWD) antibiotic-
resistant bacteria live within the 
cytoplasm of cells, including the phagocytic cells (e.g. monocytes, macrophages, lymphocytes, neutrophils and polymorphonuclear cells) of the 
immune system itself. The cellular proliferation in 
Cancer is catalysed the action of the same tiny L-form bacteria. They cause the 
cell nucleus to release mRNA signaling the Th1 
cytokine cascade without the need for conventional signaling via, for example, CD4+ T-Lymphocytes. Some of these Cytokines and Chemokines, including, without limitation, Cellular Adhesion Molecule (
CAM), create the environment which allows the cellular proliferation to start, and then allows the cancerous growth to 
gain a foothold in the body. Killing these stealthy pathogens removes the environment needed to initiate and feed the cellular proliferation commonly called ‘
Cancer,’ and prevents the chronic phase of the 
disease AIDS. This invention achieves its objective partly by reducing the ability of these tiny L-form, intra-phagocytic bacteria to translate proteins within their 70S 
Ribosome. The 30S and 50S subunits of the bacterial 
ribosome are targeted both individually and collectively. Further, this invention activates the 
innate immune system with 
agonist(s) for the VDR 
Nuclear Receptor, and modulates the availability of endogenous ligands to the PPAR, GCR and CB1 receptors, conditioning the immune 
system to more easily recognize and kill these tiny bacterial pathogens.