Actin assembly on biological membranes is a poorly understood process. Phagosomal membranes could induce actin assembly in the presence of thymosin beta4 (an actin sequestering protein that inhibits nonspecific nucleation), via the barbed ends of actin filaments. Incubation of phagosomes with reagents affecting actin dynamics show that the phagosomal membranes assemble actin filaments de novo (Defacque et al, Actin assembly induced by polylysine beads or purified phagosomes: quantitation by a new flow cytometry assay, Cytometry. 2000 Sep 1;41(1):46-54). A number of unrelated bacterial species as well as vaccinia virus (ab)use the process of actin polymerization to facilitate and enhance their infection cycle (Frischknecht et al, Surfing pathogens and the lessons learned for actin polymerization, Trends Cell Biol. 2001 Jan;11(1):30-38). The bacterial pathogens Listeria monocytogenes and Shigella flexneri recruit host factors that enable them to use actin polymerization as the driving force to facilitate their spread into neighbouring cells. It is now becoming clear that other pathogens, including viruses, have developed a number of different strategies to use the actin cytoskeleton of the host to their advantage during the infection process (Higley et al, Actin and cell pathogenesis, Curr Opin Cell Biol. 1997 Feb;9(1):62-9).

Such polymer actins may be produced under oxidative stress in order to resist further damage by excess free radicals, especially the superoxide. The polymer actin and its aggregates produced by cells or macrophages under oxidative stress, cleave at different points to show up as p160, p120, p80, p45, p41 and p24. It has been shown that a precursor p53/55, which is then cleaved to p24/25 and p17/18 and the precursor protein p160 which is cleaved to p120 and p41/p45 (Ratner, L., Haseltine, W., Patarca, R.P. et al. 1985. Complete nucleotide sequence of the AIDS virus, HTLV-III. Nature 313:277-284) and possibly at p42 and p85. The later may form complexes with EBV viral parts and since B-cell receptor binds foreign material, it fails to recognize the complex as totally foreign and allows entry. Upon entry, it stays in that form in the memory B-cell until conditions emerge that both activate it while at the same time "suggest" that it could possibly proliferate and one specific such condition is when the immune system could be sufficiently suppressed.

It would thus be extremely useful to look at a possible trigger and for a trigger to satisfy both as a trigger mechanism to reactive the EBV for proliferation and a situation in which the immune system is sufficiently would be a molecule that is itself involved in oxidative stress. And it comes in the form of hydrogen peroxide. "Hydrogen peroxide has been linked to the awakening of the latent Epstein-Barr virus, which in turn has been linked to chronic fatigue syndrome and aging" James FB, The Super Antioxidants, 1998, M. Evans and Company Inc. p 19) and accelerated aging as well. Some of the early cases showed signs of accelerated aging which can be caused independently by chronic oxidative stress associated with superoxide free radical and low SOD activity.

Hydrogen peroxide has the ability to damage the master DNA template - it can break biochemical bonds. During the normal metabolic processes in cells that involve the processsing of molecular oxygen, the superoxide free radical is formed. Superoxide is an oxygen molecule with an extra electron. Under biological conditions, the main reaction of superoxide is to react with itself to produce hydrogen peroxide and oxygen, a reaction known as "dismutation". As a free radical, it can also alter the pH value in the cytoplasm and enetually alter the biocemical ruote of glucose and can also cause oxidative damage to cell membranes and affect the transport of molecules across membranes and in turn lower the production of repair proteins and the production of antibodies or antioxidant enzymes etc.

The superoxide can also be rapidly scavenged by superoxide dismustase (SOD) and this process requires the presence of copper, zinc and magnesium (from organic sources) for its production and proper functioning. One of the by-products of scavenging superoxide by SOD is the formation of hydrogen peroxide which must then be converted by catalase or glutathione peroxidase into water and oxygen. Hydrogen peroxide is not as reactive as free radicals but can cause lipid peroxidation, leading to prostrate problems and liver cancers or cardiovascular disease etc.

Accumulating hydrogen peroxide in cells is detrimental to the biochemical activities in the cell and in excess can cause cell death. If all the hydrogen peroxide formed is not quickly converted into water and oxygen, the highly reactive hydroxyl radical is produced. The toxicity of superoxide in biological systems is due to its capacity to inactivate iron-sulfur cluster containing enzymes (which are critical in a wide variety of metabolic pathways), and can undergo fenton-chemistry and generate the highly reactive hydroxyl radical as follows;

2 O2â√‚ + 2 H2O â∫‚ O2 + H2O2 + 2 OHâ√‚

The hydroxyl radical can easily destroy hydrogen bonds in molecules and it therefore has the capacity to damage DNA molecules as well, a process that can also lead to cancer cell development or suppression of immune functions. Excess free radicals can also suppress the immune system. Cells of the immune system are rich in L-form vitamin C and excess free radicals can deplete this antioxidant and suppress immune function.

Most allophatic drugs, including antibiotics are immunosuppressive and can reduce white blood cell count. The metabolism of toxic drugs and D-form chemicals, including, antibiotics produces hydrogen peroxide and can lead to the formation of the hydroxyl radical. "It is known that as we age there is a decline in brain levels of ascorbic acid. When accompanied by a similar decrease in glutathione peroxidase, we see an accumulation of H202 and hence, elevated levels of free radicals and lipid peroxidation" (Russell L. Blaylock, M.D., Not Just Another Scare: Toxin Additives in Your Food and Drink). The decrease in the other antioxidant levels can be appreciated from the fact that the L-form of vitamin can recharge alpha-lipoic acid that in turn can recharge all the other antioxidants in the natural antioxidant network. This may explain why AIDs is more prevalent in adult populations.

Excess hydrogen peroxide accumulation in cells can easily occur in persons who are malnourished or in people with low SOD scavenging activity on account of low minerals and micro-nutrients especially selenium, zinc and copper and in people with high SOD activity but low catalase and glutathione peroxide activity. Chronic or prolonged micronutrient deficiencies can therefore also lead to cancers (see: CANCER AND MICRONUTRIENTS - IS THERE A CONNECTION WORTH EXPLORING? & TOFU).

Selenium and L-cysteine are both necessary in the formation of glutathione in the body and selenium intake becomes important to indirectly prevent hydrogen peroxide accumulation in cells that could reactive EBV. Hence, daily intake of natural antioxidants (the L-form) and minerals from fruits and vegetables is important for health and explains why nutritional interventions have been reported by researchers to have benefitted the chronically malnourished victims who had AIDS symptoms.

In its dormant form, EBV remains bound as a complex with gp42 in the B-cells but sufficient hydrogen peroxide concentration can break that complex and free the EBV viral parts that become active and begin to replicate and take over the host cell. Their toxins do further damage and precipitate disease states including cancers. If sufficient oxidative on the B-cells continues to the extent that more actin polymers are produced, more B-cells will get infected but it is not a very rapid and virulent process as Gallo's HIV was made out to be and the mathematical models could not explain the differential spread or prevalence of AIDS as observed in Africa and Europe or the US. In short, AIDS associated with the (hydrogen peroxide) reactivated EBV virus or REBV-AIDS is also nothing more than a nutritional phenomenon and the answers lie in nutritional therapies and nutritional solutions in conjunction with a reduction in the ingestion of D-form chemicals and in the use of allophatic drugs.

Most individuals exposed to people with infectious mononucleosis have previously been infected with EBV and are not at risk for infectious mononucleosis. In addition, transmission of EBV requires intimate contact with the saliva (found in the mouth) of an infected person. Transmission of this virus through the air or blood does not normally occur. The incubation period, or the time from infection to appearance of symptoms, ranges from 4 to 6 weeks. Persons with infectious mononucleosis may be able to spread the infection to others for a period of weeks. However, no special precautions or isolation procedures are recommended, since the virus is also found frequently in the saliva of healthy people. In fact, many healthy people can carry and spread the virus intermittently for life. These people are usually the primary reservoir for person-to-person transmission. For this reason, transmission of the virus is almost impossible to prevent (National Center for Infectious Diseases Epstein-Barr Virus and Infectious Mononucleosis, Updated:08/25/200). Hence, optimal nutrition that provide antioxidants and micronutrients, including selenium, copper and zinc in L-form from food sources is the best protection against diseases associated with EBV infection and reactivation.