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September 05, 2006

Nutrition and Immunity - The hungry can't eat Aids messages

On 27 May 2006, the World Health Assembly passed a resolution saying that nutrition plays a major role in AIDS and that intervention that increases access to necessary nutrients be given priority by the member states and the Director-General of the World Health Organisation.


Demonstrators demand Aids treatment at the margins of the Toronto Aids Conference

In reporting this development, Paul Taylor commented:

Slowly, but surely, evidence is beginning to emerge that some senior officials within the UN may perhaps be beginning to get the message about the relationship between poor nutrition, depressed immunity, and AIDS.

Taken alongside the recent World Health Assembly resolution calling on Member States to ensure that special attention be given to integrating nutrition into all HIV/AIDS policies, this is undoubtedly good news.

Clearly, however, and bearing in mind Rugulema's statement that he would like to see "good ARV treatment programmes", there is still undoubtedly a long way to go.

This is in reference to an article on, titled 'The hungry can't eat Aids messages', which expands on the point.

Good nutrition could be the only available life prolonging alternative to people living with HIV/Aids in rural areas, a senior officer for the UN Food and Agriculture Organisation said on Thursday.

"Sick people can't farm, they can't work. Hungry people can't eat Aids messages," said HIV/Aids and food security officer Dr Gabriel Rugulema, speaking to journalists ahead of the 16th International Aids conference in Toronto which starts on Sunday.

He said people who had little access to food could not be bothered with Aids warnings. Bad nutrition depressed the immune system, resulting in a higher likelihood of contracting HIV, the faster development of Aids and subsequent death.

I have earlier reported on the importance of particular nutrients in the prevention of Aids complications, and in 'turning off' the infection. Harvard University confirmed in a research in Tanzania, that a multivitamin supplement slowed and in some cases prevented the appearance of clinical Aids symptoms. Bill Sardi says vitamin C is an immensely important nutrient for the immune compromised, and he describes the controversy in South Africa over Dr. Mathias Rath's advocacy of nutritional intervention against the spread of Aids. According to orthomolecular medicine proponents, Aids patients are depleted of selenium, a mineral with anti-viral properties, and three important aminoacids. When supplied, these nutrients can reverse symptoms, and some patients have been known to switch to "HIV negative".

Beldeu Singh, a health researcher in Malaysia, agrees that nutrition is important. Here are his comments, and an article on the Epstein-Barr virus in Aids:

- - -

About time...

Yes its about time that the UN policies on AIDS pursue a proper and biochemically logical response and practices that promote integration of nutrition into a comprehensive response to HIV/AIDS.

This is primarily because many AIDS patients do not have the virus, pointing clearly to oxidative stress in malnourished people as the actual cause factor of AIDS and even when the reactivated EBV is involved, in certain groups of people, in the destruction of parts of the immune system, it occurs in conditions of oxidative stress and more startling is the fact that when EBV viral parts 'hide' in cells of the immune system, they are reactivated by hydrogen peroxide which is a by-product of oxidative stress. So, however you look at the AIDS condition, oxidative stress is a critical factor. Logically, therefore nutritional intervention is the key and should form the basic thrust in responding to the AIDS problem.

Resolution WHA57.14 which urged Member States, inter alia, to pursue policies and practices that promote integration of nutrition into a comprehensive response to HIV/AIDS is therefore considered urgent.

The recommendations of WHO's technical consultation on nutrition and HIV/AIDS in Africa (Durban, South Africa, 10-13 April 2005), which were based on the main findings of a detailed review of the latest scientific evidence on the macronutrient and micronutrient needs of HIV-infected people, including pregnant and lactating women and patients on antiretroviral therapy, make more sense now than before these recommendations were drafted.

Based on the oxidative factor and the reactivated EBV factor for AIDS causation, noting the fact that hydrogen peroxide (a by-product of oxidative reactions in the body), I fully concur with the WHO technical note that food and adequate nutrition are often identified as the most immediate and critical needs by people living with, or affected by, the HIV/AIDS pandemic. Many of us have advocating nutritional therapies for a long time, because we did not accept the Gallo-HIV as "the probable cause of AIDS" as a result of which we were called the dissident group by the establishment that remains as the proponent of the official view that the Gallo-HIV is the cause of AIDS.

P/s I hope you recieved my article on the EPSTEIN-BARR Virus in AIDS

- - -

I have indeed received the article, and it is here for readers interested in the biochemical details...


Epstein-Barr virus, frequently referred to as EBV, is a member of the herpesvirus family and one of the most common human viruses. The virus occurs worldwide, and most people become infected with EBV sometime during their lives. In the United States, as many as 95% of adults between 35 and 40 years of age have been infected. Infants become susceptible to EBV as soon as maternal antibody protection (present at birth) disappears (National Center for Infectious Diseases Epstein-Barr Virus and Infectious Mononucleosis).

In Third World nations, most children are infected with EBV; in most industrialized nations, about 50% of the people are infected (Encyclopedia: Epstein-Barr virus, Sixth Edition, Copyright © 2006 Columbia University Press).

Symptoms of infectious mononucleosis are fever, sore throat, and swollen lymph glands. Sometimes, a swollen spleen or liver involvement may develop. Heart problems or involvement of the central nervous system occurs only rarely, and infectious mononucleosis is almost never fatal. There are no known associations between active EBV infection and problems during pregnancy, such as miscarriages or birth defects. The symptoms of infectious mononucleosis usually resolve in 1 or 2 months.

The problem with the EBV is that it remains latent in the body and can be reactivated giving rise to latency diseases. EBV remains dormant or latent in a few cells in the throat and blood for the rest of the person's life. Periodically, the virus can reactivate and is commonly found in the saliva of infected persons. This reactivation usually occurs without symptoms of illness. This may probably be the case in people who are not malnourished.

In immunosuppressed or immunocompromised individuals, EBV can cause (fatal) lymphoproliferative disease. In contrast, in healthy individuals, EBV is well controlled by the immune system. The widespread and mostly asymptomatic persistent EBV infections in adults reflect the balance between viral replication and host immune control (Maaike E. Ressing et al, Epstein-Barr Virus gp42 Is Posttranslationally Modified To Produce Soluble gp42 That Mediates HLA Class II Immune Evasion, Journal of Virology, January 2005, p. 841-852, Vol. 79, No. 2).

"Recent studies have shown that EBV also is associated with B-cell malignancies such as Hodgkin's lymphoma (HL) and lymphoproliferative disease in immunosuppressed patients, as well as with some T-cell lymphomas and other epithelial tumors such as gastric cancers. These tumors are characterized by the presence of multiple extrachromosomal copies of the viral genome in tumor cells and the expression of part of the EBV genome" (WHO; Epstein-Barr Virus, Initiative for Vaccine Research (IVR), 2006)).

The cause of alarm stems from the fact that "EBV also establishes a lifelong dormant infection in some cells of the body's immune system. A late event in a very few carriers of this virus is the emergence of Burkitt's lymphoma and nasopharyngeal carcinoma, two rare cancers that are not normally found in the United States. EBV appears to play an important role in these malignancies, but is probably not the sole cause of disease" (National Center for Infectious Diseases Epstein-Barr Virus and Infectious Mononucleosis).

It is important to note that EBV is not the sole cause of lymphomas and carcinomas and possibly Hodgkin's disease, chronic fatigue syndrome and accelerated aging and could possibly trigger multiple sclerosis. Perhaps its reactivation is triggered in malnourished people and in people exposed to certain toxic chemicals suggesting an underlying biochemical mechanism common to both situations.

Infection with EBV is characterized by fatigue and general malaise. Infection with EBV is fairly common and is usually a transient and minor thing. However, in some individuals EBV can trigger chronic illness, including immune and lymphoproliferative syndromes. It is a particular danger to people with compromised immune systems, such as from AIDS (, Definition of Epstein-Barr virus, 1996-2006 MedicineNet).

EBV is a herpesvirus that is the major cause of infectious mononucleosis and is associated with a number of cancers, particularly lymphomas in immunosuppressed persons, including persons with AIDS. Epstein-Barr is a ubiquitous virus, so common that it has been difficult to determine whether it is the cause of certain diseases or whether it is simply there as an artifact (Encyclopedia: Epstein-Barr virus, Sixth Edition, Copyright © 2006 Columbia University Press).

How was the virus discovered? (ref: Nova Science in the News, Australian Academy of Science, Nov 1997).

In 1961, a surgeon working in Uganda, Denis Burkitt, presented the results of his research to staff at the Middlesex Hospital Medical School in Britain. He reported that the incidence of a certain tumour in African children had a geographic distribution corresponding to rainfall and temperature patterns.

The disease, which affects about 8 in every 100,000 children in parts of Africa and Papua New Guinea, quickly became known as Burkitt's lymphoma. The influence of climate on its incidence seemed to suggest that some biological factor was involved. Three researchers, M.A. Epstein, Y.M. Barr and B.G. Achong, immediately began looking for possible cancer-causing viruses in samples of the tumour sent from Uganda to Britain.

In 1964, they identified the culprit using an electron microscope: a previously unknown member of the herpes family of viruses. Epstein and Barr were awarded the dubious honour of having the pathogen named after them.

AIDS sufferers also have reduced immunity and some AIDS patients also suffer from oral hairy leukoplakia, a condition involving considerable replication of the Epstein-Barr virus in cells along the edge of the tongue. And since Burkitt's lymphoma is prevalent in countries that have high incidence of malaria, researchers have suggested that malaria infection may also play a role in reactivating EBV by possibly suppressing the immune system. The real reason perhaps may be suppression of superoxide dismutase (SOD) activity in malaria patients rather than something peculiar to malaria as "patients with immunodeficiency, either congenital or acquired (for example after immunosuppressive treatment for organ transplantation or human immunodeficiency virus (HIV) infection) have a much higher risk of developing EBV or HHV-8 associated tumours than the general population, pointing to the crucial role of the immune system in controlling the proliferation of EBV or HHV-8 infected cells" (H-J Delecluse et al, The genetic approach to the Epstein-Barr virus: from basic virology to gene therapy, J Clin Pathol: Mol Pathol 2000; 53:270-279).

Research has found that all of the lymphomas associated with AIDS and most lymphomas in other immunocompromised persons are connected with latent EBV infection. EBV has been found in biopsy tissue of patients with Hodgkin's disease, breast cancer, and some smooth muscle tumors. EBV also was formerly suspected as the cause of chronic fatigue syndrome (originally named chronic EBV syndrome) (Encyclopedia: Epstein-Barr virus, Sixth Edition, Copyright © 2006 Columbia University Press).

EBV infection seldom lasts for more than 4 months. When such an illness lasts more than 6 months, it is frequently called chronic EBV infection. However, valid laboratory evidence for continued active EBV infection is seldom found in these patients. The illness should be investigated further to determine if it meets the criteria for chronic fatigue syndrome...(National Center for Infectious Diseases Epstein-Barr Virus and Infectious Mononucleosis).

Chronic fatigue symdrome results from low ATP output from mitochondria that have suffered oxidative damage and mDNA depletion associated with free radical stress and quite possibly in people with low Co-enzyme Q10 production. This enzyme is important in the process of utilization of ATP molecules for cellular energy and excess free radicals can disrupt the 17-step process for its production in cells (see: Are Malnutrition and Oxidative Stress the Cause of gp41, gp120 and gp160 in Robert Gallo's HIV Isolate?, & HIV-Aids: A Tragic Error - Health Supreme, & Are AIDS, CFS Caused By Oxidative Damage?).

EBV is kept in check by a healthy immune system but its dormancy within the immune system is rather interesting and provides a direct link between the reactivated EBV, immunesuppression and the progression of AIDS as the Epstein-Barr virus appears capable of infecting only two major cell types: the outer (epithelial) cells of the salivary gland, and white blood cells known as B lymphocytes (B-cells) and infection of B-cells by the virus results in its proliferation as the antibodies cannot bind with it in the B-cells and the T-cells cannot attack the infected B-cells (see: Nova Science in the News, Australian Academy of Science, Nov 1997). If this explanation holds true, it offers a insight into Reactivated EBV-AIDS or REBV-AIDS and further rules out the Gallo HIV virus that is supposedly a virulent pathogen that specifically targets the immune system that was stated to be "the probable cause of AIDS".

"These are complex enveloped DNA viruses, which multiply in the nucleus of the host cell. EBV infects resting human B-lymphocytes and epithelial cells, multiplies in the latter and establishes latent infection in memory B-lymphocytes. Thus, infected individuals may produce virions, carry virus-specific CTLs, produce EBV-specific antibody, and yet harbor latently infected memory B-cells. These maintain the latent EBV genome as an episome that expresses only part of its genetic information, including EBV nuclear antigens EBNA-1 (a latent DNA replication factor), EBNA-2 (a transcriptional activator) and EBNA-3A and -3C (involved in the establishment of latency), together with integral membrane proteins LMP-1 and LMP-2 which play major roles in maintenance of latency and escape from the immune response of the host. Latently infected cells do not produce the B7 coactivator receptor and, therefore, are not killed by CTLs. When peripheral blood from an infected individual is cultured, latently infected B-cells begin to replicate and yield immortalized progeny lymphoblasts that can be indefinitely propagated in the laboratory" (WHO/IVB/05.XX; Viral Cancers).

The Epstein-Barr virus (EBV) resides as a persistent infection in human leukocyte antigen (HLA) class II+ B lymphocytes and is associated with a number of malignancies. The EBV lytic-phase protein gp42 serves at least two functions: gp42 acts as the coreceptor for viral entry into B cells and hampers T-cell recognition via HLA class II molecules through steric hindrance of T-cell receptor-class II-peptide interactions (Maaike E. Ressing et al, Epstein-Barr Virus gp42 Is Posttranslationally Modified To Produce Soluble gp42 That Mediates HLA Class II Immune Evasion, Journal of Virology, January 2005, p. 841-852, Vol. 79, No. 2).

Hutt-Fletcher and her colleague Corina M. Borza recently published their study and some unexpected observations in the June Nature Medicine. In laboratory dishes, epithelial cells are a bit more easily infected by Epstein-Barr virus that was first grown inside B cells than by virus previously grown in epithelial cells. Even more dramatic, Hutt-Fletcher and Borza found that Epstein-Barr virus grown inside epithelial cells is 30 to 100 times more efficient at infecting B-cells than the virus grown in B cells themselves. This suggests an interesting difference in form between the two.

Molecules on the virus' surface that the virus uses to gain access to cells might explain this phenomenon. To infect epithelial cells, Epstein-Barr virus seems to depend upon a complex of two proteins, gH and gL. But to get into B cells, the virus needs a third protein, gp42, in the complex. The virus typically has both types of complexes on its surface, but their ratio influences the virus' preference for one cell or another. EBV virus grown in epithelial cells has more gp42-containing complexes than virus grown in B cells (Borza, C.M., and L.M. Hutt-Fletcher. 2002. Alternate replication in B cells and epithelial cells switches tropism of Epstein-Barr virus. Nature Medicine 8(June):594-599) and that enables them to gain entry into the B-cells of the immune system.

In general, no virus is produced during latent infection, but in a certain proportion of EBV infected cells, a reactivation of the viral lytic programme can be observed, with the release of mature infectious virions (Sugden B. Expression of virus-associated functions in cells transformed in vitro by Epstein-Barr virus: Epstein-Barr virus cell surface antigen and virus-release from transformed cells. In: Purtilo DT, ed. Immune deficiency and cancer. New York: Plenum Press; 1984:165-77).

Although EBV encodes as many as 11 glycoproteins, efficient entry of EBV into B cells requires only 5 glycoproteins: gp350/220, gH, gL, gB, and gp42 (Amanda L. Silva et al, Mutational Analyses of Epstein-Barr Virus Glycoprotein 42 Reveal Functional Domains Not Involved in Receptor Binding but Required for Membrane Fusion, JOURNAL OF VIROLOGY, June 2004, p. 5946-5956).

Ressing et al, demonstrated that the gp42 protein functions as an immune evasion molecule for HLA class II-restricted T-cell responses (Ressing, M. E., 2003. Interference with T cell receptor-HLA-DR interactions by Epstein-Barr virus gp42 results in reduced T-helper cell recognition. Proc. Natl. Acad. Sci. USA 100:11583-11588) and that spefically allows its entry into the B-cells of the immune system and from there it can proliferate wildly if reactivated producing toxins that precipitate disease conditions.

The toxins of the reactivated and proliferating EBV in all likelihood cause damage to tissues in any system of the body. When its toxins concentrate in the endothelium and cause endothelial dysfunction, the excess NO could result in multiple sclerosis and if the NO reacts with ROS forming the reactive peroxynitrite free radical, other disease states could develop. An interesting hypothesis is that its toxins may damage the oxygen molecule to produce the superoxide radical thereby producing the twin effects of;

1. Firstly, a feeling of tiredness and general mailaise, and

2. Damaging cell membranes and altering the pH value in the cytoplasm by increasing the acidity that in turn inactivates the enzymes involved in the Krebs cycle causing a drop in ATP output and finally leading to the rerouting of glucose into the glucose-alcohol (anaerobic) pathway that transforms the cell into a cancer cell.

This biochemistry fits into the view of EBV associated diseases, including tiredness, general malaise, chronic fatigue and AIDS. Equally AIDS can develop through oxidative stress alone, especially in malnourished people and when both factors are taken together, a mathematical model would more accurately describe the prevalence of AIDS from African countries to the developed nations. In African countries such as Uganda, in the lymphoma belt, the association of BL with EBV is very strong (97%), whereas it is weaker elsewhere (85% in Algeria; only 10 to 15% in France and the USA).

So, two critically important questions must be answered. First, how does EBV selectively infect memory B-cells in humans and secondly what triggers the reactivation of EBV that lies dormant in the B-cells of the human immune system?

In vitro culture of rat natural killer (NK) cells in high concentrations of recombinant interleukin 2 (rIL-2) leads to the expression of a surface glycoprotein with a molecular mass of approximately 42 kD. This glycoprotein, gp42, is not induced on other lymphocytes and thus provides a lineage-specific marker for rIL-2- activated NK cells (WE Seaman, Molecular cloning of gp42, a cell-surface molecule that is selectively induced on rat natural killer cells by interleukin 2: glycolipid membrane anchoring, and capacity for transmembrane signaling, Journal of Experimental Medicine, Vol 173, 251-260, Copyright © 1991 by Rockefeller University Press). Thus, gp42, the only NK-specific activation antigen, is a GPI-anchored surface molecule with the capacity to re-enter the NK cells and if it binds with another agent or molecule or viral parts, the entire complex can enter the NK cells and the gp42 glycoprotein serves as an immune-evasion mechanism to the whole gp42-viral complex in rats.

Recent reports suggest that the EBV infection is closely associated with mature natural killer (NK) cell malignancies in humans, too but there has been no direct evidence that EBV infects human NK cells in vitro (ref: Yasushi Isobe, Epstein-Barr Virus Infection of Human Natural Killer Cell Lines and Peripheral Blood Natural Killer Cells, Immunology, Cancer Research 64, 2167-2174, March 15, 2004).

Whereas, viral glycoproteins, gp42 and gp85, are known to play an important role in EBV internalization into HLA class II-positive cells (Molesworth SJ et al, Epstein-Barr virus gH is essential for penetration of B cells but also plays a role in attachment of virus to epithelial cells. J Virol, 74: 6324-32, 2000: Borza CM and Hutt-Fletcher LM. Alternate replication in B cells switches tropism of Epstein-Barr virus. Nat Med, 8: 594-9, 2002), oxidative stress caused by superoxide free radicals may be the facilitating factor that allows entry of EBV into human NK cells.

The issue in human EBV infection, however, is in large proportion related to B-cell infection. The key to explaining EBV infection in humans lies in oxidative stress on the cell membrane of B-cells and the consequent decline of oxygen in the cell. The process of phagocytosis requires the polymerization of actin in a directional fashion to surround and internalize the target. Actin polymerization is dependent on adequate supplies of ATP. Exposure to hyperoxia can impair the activity of cellular enzymes important in oxidative metabolism, which could lead to increased anaerobic glycolysis, depletion of glucose in the cell growth medium, and subsequent depletion of ATP. However, ATP levels in RAW 264.7 cells cultured in hyperoxia were not reduced. Glucose content in the cell growth medium was higher in the hyperoxic cultures, likely as a result of inhibition of cell proliferation by hyperoxia. Examination of the actin cytoskeleton of RAW 264.7 cells cultured in hyperoxia, by immunofluorescence microscopy, revealed marked changes, including an increase in the degree of actin polymerization, loss of cortical actin, and the formation of prominent stress fibers and actin aggregates (see Philip J et al, Hyperoxia Impairs Antibacterial Function of Macrophages Through Effects on Actin, American Journal of Respiratory Cell and Molecular Biology. Vol. 28, pp. 443-450, 2003).

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.

Hydrogen Peroxide

It would thus be extremely useful to look at a possible trigger and for a trigger to satisfy both as a trigger mechanism to reactivate the EBV for proliferation and a situation in which the immune system is sufficiently weakened 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 biochemical route 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 prostate 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 (see:Activation Of Oxygen: 1996, Oxidative Stress, Dr. Bryan D. McKersie, University of Guelph) as follows;

*O2 + H2O2 ----> O2 + .OH + OH-

This is a well known reaction in Fenton chemistry caused by the superoxide as a reducing agent. 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 stress 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.

There is a strong scientific and commercial focus on developing vaccines and immunotherapeutic strategies for the treatment of EBV-associated diseases. The problem with developing a vaccine for EBV-associated diseases arises primarily from the fact that the viral parts of this virus 'hide' in cells of the immune system and this viral part can be reactivated in certain conditions.

The wide range of EBV latency diseases can be primarily on account of the possibility that the size of the viral parts that 'hide' vary but they contain enough genetic information to cause a variety of EBV-associated disease, upon becoming reactivated. For this basic reason, it is unlikely that a single vaccine that is applicable to all EBV-associated diseases could not be developed. Given the variety of potential EBV targets, its latency diseases presented problems of immune recognition of latency diseases and vaccine development.

If the link between the reactivated EBV and AIDS, based on oxidative stress as the key factor in reactivating it through hydrogen peroxide as the chemical that the EBV viral-part bond with the polymer actin is to be tested by theoretical biology, one would expect a higher incidence of AIDS among alcohol abusers, cigarette smokers and crack-smokers as well as in poor communities.

Researchers led by Brian R. Edlin of the Centers for Disease Control and Prevention, examined drug use in New York, Miami, and San Francisco have found that crack cocaine is "helping" to spread HIV to heterosexuals in poor, inner-city communities. Desperate for a new "hit," crack addicts are selling sex in exchange for drugs or money. The result is that HIV is spreading through the communities, particularly among women. Among the participants in New York and Miami, AIDS was 2.3 times more prevalent among crack smokers than among non-smokers (Washington Post (11/24/94) P. A24:cf, Prevention News Update).

A second test would be to find out if older drug users have a much higher prevalence of AIDS, simply because the antioxidant levels in the body decline with age. By 40 years of age, the blood antioxidant levels, in general drop by about 50% which means that the prevalence rate would be more than doubled in older groups as they would be more likely to suffer oxidative stress than younger counterparts. "The numbers of older drug users are increasing, and several issues have been identified that differentiate them from their more frequently studied younger counterparts. Approximately 11 percent of all AIDS cases diagnosed through 1999 have occurred among adults 50 years or older, a figure that has been fairly consistent since the epidemic began (Carol and Roberts, HIV Risk Behaviors Among Older American Drug Users, Journal of Acquired Immune Deficiency Syndromes (06.01.03) Vol 33; Suppl.2: P. S131-S137).

Another way to further test, would be to first theorize that AIDS patients who are cigarette smokers and categorized as abdominally obese would also have a higher incidence of other free radical induced illnesses such as cardiovascular disease. Dr. Genevieve Chene, from Universite Victor Segalen Bordeaux 2 in France, and colleagues found that men with AIDS were more likely to smoke, have a higher waist-to-hip ratio, and a higher triglyceride level than the men in the comparison group. Similar trends were seen women with AIDS, but they had higher total cholesterol levels than did women in the comparison group. The researchers reported that the estimated five-year risk of developing coronary heart disease was 20 percent higher than the general population among HIV-infected men, and 59 percent higher among women with AIDS (see:HIV Patients Have More Heart Disease Risk Factors, Reuters Health (07.24.03), VA HIV/Hepatitis C News Service). So, basically, the prevalence of AIDS is higher among individuals who are more likely to suffer oxidative stress.

AIDS prevalency rates vary between 3% and 12% among heterosexuals among male and female alcohol inpatients and outpatients from varying racial/ethnic backgrounds. Excess alcohol intake and alcohol abuse can lead to oxidative stress, and individuals who fall in this category would be predicted to have a higher prevalence rate of AIDS than the general population, primarily on account of higher prevalence of oxidative stress.

The idea presented in this article explains the hiding mechanism in cells of the immune system and its latency on account of the binding of EBV viral parts after primary infection of the epithelial cells and clearly illustrates the biochemical basis and mechanism of its liberation from the actin polymer, upon which it becomes reactivated to produce its latency diseases. Biochemical mechanism is through 'excess' hydrogen peroxide asociated with oxidative stress.


posted by Sepp Hasslberger on Tuesday September 5 2006
updated on Monday December 13 2010

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Readers' Comments

Recovered comment (some of them got swallowed up by the system)...

Keeping in mind the main striking and key aspects in the AIDS disease condition as follows:

1. "The "Gallo-HIV" replicates in 24 hrs, just like other human viruses - the latent period for HIV-caused AIDS should be the same as that of other viruses, like flu or measles, namely days to weeks. But it is 5-10 years - just about equal to the "latent periods" for lung cancer from smoking or liver cirrhosis from drinking (A Startling Claim about the AIDS Virus;By Ostap Karmodi The Moscow News;interview with Duesberg).

2. The "spread" of AIDS is not exactly random but it certainly does not follow the patterns of a disease spread by a virus and certainly not one that targets the immune system of cells of the immune system. The HIV=AIDS scientists claimed that "after entering the body, the virus rapidly disseminates, proceeding to the lymph nodes and related organs where it replicates and accumulates in large quantities". Yet, it won't fit into a mathematical model of such aggressive virulence. So, the question it the "spread" of AIDS or its prevalence that we should be talking about?

3. "The AIDS epidemic in the US and Europe has increased slowly during the decade from the early '80s to the early '90s and has since declined slowly - unlike any new microbial epidemic in history, but very much like chemical epidemics such as lung cancer from smoking or tuberculosis from cocaine"(A Startling Claim about the AIDS Virus;By Ostap Karmodi The Moscow News;interview with Duesberg). Chronic benzene poisoning results in great individual variation in signs and symptoms and includes lymphomas, myeloid leukemia, Hodgkin's disease etc., much like in AIDS and mutagenesis due to severe free-radical damage. The cumulative effect of benzene and its derivatives takes a few to several years to develop and manifest, in most cases up to 10-12 years.

4. The presence of AIDS in developed countries and regions (eg US and Europe) is very different from the very poor societies as in African communities and communities in the sub-sahara. While in the first group, the oxidative stress is linked to chemical-stressors and the use of chemicals or the abuse of chemical substances, in the later group of people, the very low intake of antioxidants, including low intakes of natural vitamin A and C and low intake of selenium and antioxidant oils provides the link to oxidative stress and oxidative injury. Cell walls and cell membranes that have suffered oxidative injury tend to promote viral entry and/or tend to inhibit healthy biochemical pathways. And the later group is exposed to diseases like malaria that create further oxidative stress in the bloodstream. An exception is found in Senegal where the soils are rich in selenium - a factor that coincides with relatively very low AIDS incidence. A virulent pathogen would spread in very similar patterns in both affluent and the very poor communities.

5. People sufferring from chronic or prolonged malnutrition or those infected with malaria and are recovering have lower blood antioxidant levels when matched for the same age group in affluent societies and that means a relatively weakened antioxidant defense mecahnism. Malaria and chronic malnutrition are most common in Africa.

So, although in the United States, as many as 95 of adults between 35 and 40 years of age have been infected with EBV and in most industrialized nations, about 50 of the people are infected with EBV, the populations in these regions enjoy much better nutrition and are therefore less likely to suffer oxidative stress from chronic malnutrition to the extent that could reactivate the EBV viral genome. This is in sharp contrast to individuals who abuse drugs and alcohol and other chemical stressors as in anal sex that can dramatically increase the risk of oxidative stress to yield sufficient available hydrogen peroxide and hydroxyl radicals to break the actin-viral bond to liberate the viral genome that could contain sufficient information to be infective and able to produce latency diseases. Accordingly, the prevalence of AIDS in such groups and in African populations will be strikingly different when compared to populations in the more affluent regions that also have greater awareness of the role of nutrition in health and have much higher daily intakes of antioxidants. The model conforms more suitably to AIDS as a latency illness caused by a reactivated viral part of EBV wherein such reactivation is caused by hydrogen peroxide and hydroxyl radicals associated with oxidative stress.

Posted by: ??? on October 6, 2006 06:42 AM


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