Are AIDS, CFS Caused By Oxidative Damage?

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11 Oct 2005 17:40:02 -0000

Health Supreme Update: Are AIDS, CFS Caused By Oxidative Damage?

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Health Supreme Update: Are AIDS, CFS Caused By Oxidative Damage?

 

 

 

 

2005.10.11 19:40:01

 

 

 

 

Are AIDS, CFS Caused By Oxidative Damage?

 

 

The officially supported theory of AIDS as an illness caused by a

continually mutating retrovirus called HIV has not led to progress in

controlling the epidemic in over two decades. We are still looking for

a vaccine but chances are it will never be found. We are still

treating those reacting positively to a non-virus-specific test with

toxic medications, but the results are less than brilliant.

 

The existence of long-term AIDS survivors is unexplained and

unexplainable, unless we look for alternative explanations of what

might cause the immune weakness observed in AIDS patients. Since the

virus has never been properly isolated and since the so-called HIV

test does not prove infection, it follows that something else must be

wrong with those unfortunate people who have a compromised immune system.

 

In the following article titled Vaccines, Antibodies and the HIV

Riddle, Beldeu Singh introduces a hypothesis of oxidative causation of

immune weakness. The new hypothesis overcomes problems associated with

proving viral causation of the syndrome but it also opens a door to

specific treatments that could rapidly reverse the epidemic.

 

- - -

 

VACCINES, ANTIBODIES AND THE HIV RIDDLE

 

The human immune system is a complex and amazing array of response

mechanisms to foreign bodies called antigens designed to attack and

destroy them and prevent infection and disease condition.

 

The system is remarkably effective to antigens. An antigen is any

substance that elicits an immune response, including a virus and parts

of broken protein molecules. Non-living substances such as toxins,

chemicals and drugs can be antigens.

 

Acquired Immunity

 

The effectiveness of the immune system is based on four very important

aspects of its design and operation - firstly, its role in

self/non-self recognition; secondly, it ability to produce a wide

range of antibodies but each antibody is a specific response to an

invading antigen, so it is in fact a polyclonal system that develops

monoclonal responses; thirdly, its antibodies bind to specific

antigens not only at the initial site of invasion or infection but

work in all the fluid part of the body and fourthly, the bodies can

stay on after overcoming the infection for months or years and in the

case of viral infections they offer live long immunity.

 

Most invasions by microorganisms do not result in disease. The few

microbes that manage to cross the barriers of skin, mucus, cilia, and

pH are usually eliminated by the natural or innate immune mechanisms

that are triggerred immediately upon pathogen entry. If the pathogen

cannot be rapidly eliminated by phagocytosis, inflammation is induced

with the synthesis of cytokines and acute phase proteins. This early

induced response is not antigen-specific and does not generate immune

memory. Only if the inflammatory process is unsuccessful at

eliminating pathogen will the adaptive immune system be activated - as

in the case of catching a cold and process will require several days

to produce armed effector cells.

 

Parts of the immune system are antigen-specific and have memory. The

cells recognize and mount an even stronger attack to the same antigen

the next time. The self/non-self recognition is on account of having

every cell display a marker based on the major

histocompatibility complex (MHC). Any cell not displaying this marker

is treated as non-self and attacked. The process is so effective that

undigested proteins in the bloodstream are treated as antigens.

 

Active artificially acquired immunity refers to any immunization with

an antigen. By giving a safe form of the antigen artificially, the

body will produce its own antibodies and, more importantly, develop

circulating, long-lived B-memory cells with high affinity B-cell

receptors on their surface. If at a later date the body is again

exposed to that same antigen, the memory cells will cause immediate

and rapid production of the appropriate antibodies for protection.

 

The immune system is a system of specialized cells and organs that

protect an organism from invasion and infection from bacteria, viruses

and it also destroys cancer cells and foreign bodies and even elicits

an immune response to broken protein molecules or those protein

molecules that may be broken during the process of ingestion by

macrophages and may float in the bloodstream as macrophage debris.

 

The organs of the immune system, positioned throughout the body, are

called lymphoid organs. The lymphoid tissue is distributed in many

other locations as small pockets throughout the body, such as the bone

marrow and thymus. The tonsils, adenoids, Peyer's patches, and the

appendix are also lymphoid tissues.

 

Antigens and Antibodies

 

An important organ of the immune system is the spleen. In it are found

B cells, T cells, macrophages, dendritic cells, natural killer cells

and red blood cells. In addition to capturing foreign bodies

(antigens) from the blood passing through it, migratory macrophages

and dendritic cells bring antigens to the spleen via the bloodstream.

An immune response can be initiated in the spleen when any macrophage

or dendritic cells present the antigen to the appropriate B or T

cells. The B cells become activated and respond with the production of

large amounts of antibody specific to the antigen. The spleen can be

visualized as an immunologic filter of the blood.

 

A healthy immune system, functioning at its optimal levels keeps the

body in a healthy state. If the immune system weakens, its ability to

defend the body also weakens, allowing pathogens, including viruses

that cause common colds and flu, to grow and flourish in the body. The

immune system also performs continual surveillance for abnormal or

cancer cells. Any form of prolonged immune suppression compromises the

healthy functioning of the immune system and allows opportunistic

infections, including TB, pneumonia and cancers to occur in the body.

Immunosuppression has been reported to increase the risk of certain

types of cancer.

 

The immune system can be made to elicit an immune response

artificially. Active artificially acquired immunity refers to any

immunization with an antigen. By giving a safe form of the antigen

artificially, the body will produce antibodies. Viral vaccines such as

for small-pox can cause the immune system to develop circulating,

long-lived B-memory cells. If at a later date the body is again

exposed to that same antigen, the memory cells will cause immediate

and rapid production of the appropriate antibodies for protection.

 

Most vaccine-preventable diseases are caused by viruses. Vaccines to

help prevent these diseases generally contain weakened or killed

viruses specific to the disease. There are a series of steps that the

body goes through in fighting these diseases: First, a vaccine is

given by a shot. Next, over the next few weeks the body makes

antibodies and memory cells against the weakened or dead viruses in

the vaccine. Then, the antibodies can fight the real disease-causing

viruses in the person.The antibodies destroy the viruses and the

person will not become ill. We learnt that in school.

 

We also learnt in school that an antibody is a protein produced by the

immune system, in response to invading or foreign bodies introduced

into the body, to identify and neutralize these foreign bodies such as

bacteria and viruses. Each antibody recognizes a specific antigen

unique to its target.

 

Antibodies are synthesized and secreted by plasma cells which are

derived from the B cells of the immune system. The B cells are

activated upon binding to their specific antigen and differentiate

into plasma cells that will produce the immunoglobulins (which are

glycoproteins in the immunoglobulin superfamily) that function as

antibodies.

 

Antibodies are therefore produced in clonal lines that are specific to

only one antigen, e.g., a virus hull protein. In binding to such

antigens, they can cause agglutination and precipitation of

antibody-antigen products ready for phagocytosis by macrophages and

other cells or block viral receptors and stimulate other immune

responses such as the complement pathway.

 

Antibodies that bind onto the docking sites of viruses block their

docking ability to receptor sites on cell membranes. Being unable to

dock to a cell, they cannot infect it. Antibodies can also agglutinate

them so the phagocytes can capture them. Antibodies that recognize

bacteria mark them for ingestion by macrophages. Activated macrophages

are also capable of directly destroying tumor cells. Together with the

plasma component complement, antibodies can kill bacteria directly.

Antibodies also neutralize toxins by binding with them.

 

Antibodies are found in the blood and tissue fluids. In some cases

they may be aided by T-helper cells to fight foreign bodies. They

cannot attack pathogens within cells. Certain viruses " hide " inside

cells (as part of the lysogenic cycle) for long periods of time and

avoid the binding action of antibodies. The chronic nature of many

minor skin diseases (such as cold sores) is due to this " hiding "

mechanism. Any further outbreak is quickly suppressed by the immune

system, but the infection is never truly eradicated in such cases

because some cells retain viruses that may resume their replicating

activity later on.

 

Antibodies and memory cells stay on guard in the body for years after

the vaccination to safeguard it from the real disease germs. This

protection is called immunity.

 

In the case of all bacterial vaccines, immunity doesn't last long and

thus the vaccine needs frequent repetition to be effective, which

means you are exposed to the risk again and again, unlike viral

vaccines which provide years, probably a lifetime, of immunity.

 

Cancer Immunotherapy

 

Humans and mammals, including dogs, cats and mice have the ability to

make antibodies that 'recognize' virtually any antigenic determinant

(epitope) and bind to it. Additionally, antibodies are so specific

that they discriminate between even similar epitopes. These two

characteristics provide the basis for protection against disease

organisms and make antibodies attractive candidates to target other

types of molecules found in the body, such as: receptors or other

proteins present on the surface of normal cells molecules or that may

be present uniquely on the surface of cancer cells.

 

Monoclonal antibodies can be produced in a laboratory. Monoclonal

antibodies are made by injecting human cancer cells, or proteins from

cancer cells, into mice so that their immune systems develop

antibodies against the injected foreign antigens (bodies). These new

antibodies will bind to specific proteins on the surface of certain

cells and T4 cells can identify them easily and attack them. Once

bound, the cancer cells are marked for destruction by macrophages and

the binding action activates the immune system to attack and kill the

cells to which the monoclonal antibody is bound. It is an interesting

approach in immunotherapy.

 

There are clearly identified processes in immunotherapy that destroy

cancer cells. In one process, macrophages and natural killer cells

engulf the bound tumor cell. Macrophages destroy cancer cells by

ingestion using enzymes while natural killer cells secrete cytokines

that lead to cell death. In the second process, when the " complement

system " is initiated, also known as the 'complement cascade', the

attack is confined to the cell membrane of the cancer cell resulting

in a hole within the cell membrane, causing cell lysis and death of

the cancer cell. Natural killer cells have a smart mechanism to kill

infected cells. They insert the pore-forming molecule perforin into

the membrane and then inject cytotoxic granzymes to kill the targeted

cell.

 

Before they can engulf pathogens, phagocytes must first bind them.

Pathogen surfaces generally have sugar molecules in repeating patterns

(orientation and spacing) not found on host cells that can be

recognized by cells of the innate immune system. Once the antigen is

bound, the phagocyte extends pseudopodia around the antigen and

engulfs it, forming a phagocytic vesicle (phagosome). Cytosolic

vesicles called lysosomes containing digestive enzymes at low pH fuse

with the phagosomes to become phagolysosomes, whose enzymes digest the

antigen. This process is called phagocytosis. Some bacteria are

resistant to hydrolytic enzymes and low pH and can escape from or even

live in the phagolysosome. Pathogens are generally completely digested

by neutrophils (See: Immunology;).

 

Natural killer (NK) cells function as effector cells that directly

kill certain tumors such as melanomas, lymphomas and viral-infected

cells, most notably herpes and cytomegalovirus-infected cells. Natural

killer cells, unlike the CD8+ (killer) T cells, kill their targets

directly without a prior " conference " in the lymphoid organs. However,

NK cells that have been activated by secretions from CD4+ T cells will

kill their tumor or viral-infected targets more effectively.

 

Natural killer cells are specialized cells that kill both cancer cells

and cells that are harboring viruses. Their numbers increase with

exercise, and supplementation with DHEA, thymus extract, vitamin E,

selenium, beta-carotene, glutamine, and arabinogalactan. Their numbers

fall with malnutrition, stress, alcoholism, inadequate sleep, and in

people with chronic fatigue syndrome and other illnesses (See: Immune

Response;), drug abuse and in heavy smokers.

 

In addition to their hydrolytic enzymes, phagocytes use two

oxygen-dependent killing systems (oxidative burst) to kill

microorganisms by oxidizing and inactivating key enzymes. Macrophages

depend primarily on the peroxidase-independent system, using hydroxyl

radicals (OH-), superoxide anions (O2-), singlet oxygen (O-) and

hydrogen peroxide (H2O2). Neutrophil myeloperoxidase interacts with

H2O2 plus intracellular halides to form toxic oxidants such as OCl-.

Activated macrophages also kill pathogens with nitric oxide (NO),

defensin peptides, lysozyme, and secreted molecules that compete with

the microbes for essential nutrients such as iron and the enzyme

cofactor vitamin B12. Toxic products of macrophages and neutrophils

can be used inside the phagolysosome to kill the pathogen or, when the

pathogen cannot be engulfed, can be excreted for extracellular

killing. The latter process often results in damage to surrounding

host cells as well as to the pathogen (See: Immunology;).

 

Nitric oxide (NO) has broad-spectrum antimicrobial properties and is

also synthesised by the endothelium of the major blood vessels.

Endothelial health and secretions of NO in proper amounts is a science

that will gain prominence in developing future therapies and will

become a vital concept in health. It is an ubiqutious molecule in

mammalian biochemistry and is involved in the development of disease

states.

 

Cancer cells may spread into the central nervous system, testicles or

other organs not easily reached with chemotherapy. These areas are

often referred to as sanctuary sites. Since many drugs are unable to

penetrate into these areas and destroy the cancer cells, immunotherapy

may be applied as an alternative.

 

Cytotoxic T cells (CTL) mediate antigen-specific, MHC-restricted

cytotoxicity and are important for killing intra-cytoplasmic parasites

that are not accessible to secreted antibody or to phagocytes.

Examples include all viruses, rickettsias, some obligate intracellular

bacteria (Chlamydia) and some protozoan parasites. The only way to

eliminate these pathogens is to kill their host cells. Activated T

cells perform their effector functions when they encounter

MHC-presented peptide on their target cells. Cytotoxic T cells

activated by endogenous antigen, identify and kill the infected cells

while helper T cells are activated by exogenous antigen to stimulate

macrophage killing of endosomal pathogens.

 

Vaccination and Autoimmune Disease

 

The remarkable specificity of antibodies makes them interesting for

study in medical science. The response of the immune system to any

antigen, even the simplest, is polyclonal, which means, the immune

system produces antibodies of a great range of structures both in

their binding regions as well as in their effector regions. Hence, the

interest in vaccines.

 

Vaccines have been useful in preventing viral diseases such as

small-pox but vaccines pose challenges of their own. There is some

evidence to suggest to even the most ardent vaccine supporter that

there are risks to vaccination. The only thing that does immunize

(i.e. enable the body to protect itself from harm by foreign

organisms) is Mother Nature, provided she is properly supported with

sufficient basic nutrition, and her sophisticated immune development

process not interfered with (Vaccination Information Service;).

 

The term " immunisation " , often substituted for vaccination, is false

and should be legally challenged, because the direct injection of

foreign proteins and other toxic material (particularly known

immune-sensitising poisons such as mercury) sensitises, meaning makes

the recipient more, not less, easily affected by what he/she

encounters in the future. This means they do the OPPOSITE of immunise,

commonly even preventing immunity from developing after natural

exposure. (Vaccination Information Service;).

 

According to leading canine vaccine researcher Dr. Ronald Schultz,

Chair of the Department of Pathobiology at the University of Wisconsin

- Madison School of Veterinary Medicine, and editor of the textbook

Veterinary Vaccines and Diagnostics, It is becoming increasingly more

evident that it is no longer true to say, 'Well, even if the vaccine

doesn't help, it won't hurt.'

 

A few years ago, the Colorado State University School of Veterinary

Medicine became the first veterinary college to issue a vaccination

schedule that recommended against annual vaccinations. Of particular

note in this regard has been the association of autoimmune hemolytic

anemia with vaccination in dogs and vaccine-associated sarcomas in

cats ... both of which are often fatal (cf Re-Vaccination: Vaccination

for Previously Vaccinated Dogs and Older Puppies By Christie Keith) " .

 

In cats, there is an alarming incidence of injection site sarcomas, an

aggressive and often fatal cancer. In dogs, there is a correlation

between autoimmune hemolytic anemia and vaccination (Dodds, 1985;

Duval and Giger, 1996), and an ongoing study at Purdue University has

found that vaccinated dogs, but not unvaccinated controls, have formed

antibodies to their own cells (Larry T. Glickman, DVM, " Weighing the

Risks and Benefits of Vaccination, " Advances in Veterinary Medicine,

Vol. 41, 2001). Immunocompromised dogs vaccinated for canine distemper

have been reported to develop post-vaccinal encephalitis (Meyer,

" Vaccine Associated Adverse Events, " Veterinary Clinics of North

America, May 2001). Dogs with inhalant allergies are known to worsen

after vaccination (Frick and Brooks, 1983; cf Re-Vaccination:

Vaccination for Previously Vaccinated Dogs and Older Puppies By

Christie Keith).

 

So, the problems that can be caused by vaccinations are autoimmune

disease conditions and vaccine associated sarcomas. It is important to

note the research that points to the fact that the direct injection of

foreign proteins and other toxic material (particularly known

immune-sensitising poisons such as mercury) makes the recipient more,

not less, easily affected by what he/she encounters in the future.

This means they do the OPPOSITE of immunise, commonly even preventing

immunity from developing after natural exposure. Since vaccines use

thimerosal, a compound containing organic mercury, subsequent

vaccinations (especially a large number of mandated vaccinations

within the first two years) cause problems not only from the free

radical generating toxicity of the mercury ion (that accumulates in

the tissues) but many may also suffer from its immune sensitizing

effect. Thimerosal in vaccines may interfere with NO secretions by

cells and in tissues and cause the wide range of problems in health.

 

But antibodies continue to interest scientists and in their possible

role in preventing developmental defects in fetuses. Cytomegalovirus,

or CMV, spreads through sex and body fluids like saliva. It often

infects children and their caregivers and is the most common infection

among U.S. newborns, striking about one per cent, or 40,000 babies

each year. It infects most people at some point, typically with mild

symptoms or none at all. But it can harm or kill fetuses and is

especially dangerous when women acquire it during pregnancy.

 

Up to 20 per cent of infected fetuses die before or soon after birth,

or have severe damage, including small heads, abnormal brains, mental

retardation, and liver and hearing damage. Others develop learning

disabilities by school age.

 

Italian doctors, in a study, injected highly concentrated antibodies

to CMV into 31 women who became infected with the virus during

pregnancy and whose fetuses were known to be infected as well. Only

three per cent had babies with CMV damage, compared with half of the

14 women who refused the treatment. A second group of 37 women whose

babies were suspected of being infected also received the treatment.

Sixteen per cent had babies with CMV damage, versus 40 per cent of

women in a comparison group who didn't get the treatment. The results

were published in the New England Journal of Medicine by researchers

at Virginia Commonwealth University .

 

Experts said it is nearly impossible to tell what helped the babies

because the women got different numbers and doses of antibody

treatments and by different methods and the most interesting question

is how physical damage to fetuses from the infection, clearly

documented in some by ultrasound, could be reversed by the antibody

treatment, given that the mothers' own CMV antibodies don't protect

fetuses from infection.

 

The answer may lie in the fact that physical damage to fetuses is

caused by developmental defects and these are in turn produced by

interference by excess free radicals or excess nitric oxide secreted

in the mother. They are very small compared to most molecules and pass

the placental barrier to cause problems in fetal development which is

primarily an environment of rapidly dividing cells. Excess free

radicals and excess nitric oxide due to endothelial dysfunction, on

account of oxidative stress on it, may be produced in mothers who

smoke or consume alcohol or in those who may have taken immuno-toxic

medication during pregnancy.

 

Since its discovery in 1980 as a potent vascular smooth muscle

relaxant and regulator of blood pressure, NO has been found in many

cell types and implicated in a variety of biological roles. Indeed, NO

is involved in the health and disease of all organs and systems,

including in the immnune system and disease prevention. Nitric oxide

is an important bioregulator of a wide variety of physiological

processes and its excess or deficiency can cause developmental defects

in fetuses and infants.

 

Many viral toxins may exert a similar effect in excess and the

administration of antibodies to viruses in pregnant mothers helps to

reduce, diminish or eliminate their stress on developing tissues and

dividing cells as the antibodies bind with the viral toxins and

neutralize them. This also explains the variable results in different

mothers. The mothers' immune system maintains a form of integrity in

the sense that it responds effectively to the invasion and threat to

its own body and produces adequate amounts of antibodies for its own

well being. The mothers' body cannot respond to the antibody

requirements in the body of the fetus and assess the additional

amounts that may be required to prevent the developmental defects in

the fetus.

 

Dr Gallo 'finds' the Virus

 

Antibodies and viruses have that interesting connection which has a

bearing on AIDS. Dr. Gallo began to put forth his claims that he had

discovered a virus (called the HIV) that he claimed was causing AIDS.

Despite the fact that those efforts in isolating viruses and

replicating them do not meet the accepted gold standard and no

scientist has proved that such a virus actually infects and replicates

in cells of the immune system, there are scientists in institutes who

claim 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. Paradoxically, the filtering

system in these lymphoid organs, so effective at trapping pathogens

and initiating an immune response, actually helps destroy the immune

system. As healthy CD4+ T cells travel to the lymph organs in response

to HIV infection, they are infected by the HIV that is harbored there. "

 

Gallo managed at the same time to file together with his employer, the

National Institutes of Health, for a lucrative AIDS test patent.

However, subsequent nucleic acid sequence analyses proved Gallo's

virus from 1984 to be the same as the virus discovered by Luc

Montagnier in 1983. Since Montagnier had sent his virus to Gallo in

1983, it appeared that Gallo had rediscovered Montagnier's virus. In

addition, a legal investigation proved that the photograph of HIV in

Gallo's first AIDS papers was that of Montagnier's virus

" inadvertently " used " largely for illustrative purposes " (p.

210-11)(On Virus Hunting; review by Peter Duesberg).

 

The story started in 1975. " By 1975 his [Gallo's] lab had finally

isolated a retrovirus from human leukemia cells. [HL23V] Gallo...

faced humilation when he presented the finding at the Virus-Cancer

program's yearly conference. Other scientists had tested his virus and

discovered it to be a mixture of contaminating retroviruses from

woolly monkeys, gibbon apes and baboons. Gallo tried to save his

reputation, speculating wildly that perhaps one of the monkey viruses

caused the human leukemia. In 1980 Gallo was finally credited for

discovering a genuine human retrovirus, HTLV-I, which he blamed for a

leukemia in blacks from the Caribbean. But he ran into trouble trying

to find the virus in American leukemia patients. At the same time, a

Japanese research team reported isolating a human retrovirus from

leukemic patients, which they named ATLV. After they courteously sent

Gallo a sample of the virus to compare with his own, Gallo published

the genetic sequence of HTLV-I. The sequence of Gallo's Caribbean

virus proved to be nearly identical to the Japanese virus; it

contained a mistake identical to the one made by the Japanese group.

Since all other non-Japanese HTLV-I isolates differed much more widely

from the Gallo-Japanese twins, some retrovirologists suggest Gallo may

have offered the Japanese sequence as his own. No formal investigation

has probed this incident, and Gallo was awarded the prestigious Lasker

Prize as the presumed discoverer of the leukemia virus. " (Inventing

the AIDS Virus, p.160).

 

" Gallo did not stop with his first human retrovirus. He isolated a

second one in 1982, from a cell line derived from a patient ... But

since that time HTLV-II has been retrieved from only one other patient

with a similar leukemia, while plenty of cases have been found without

the virus. (p.127) ... William Haseltine ... had copied the genetic

sequence of HTLV-II, the second known human retrovirus, from a

presentation at a science conference. He then published the sequence,

unknowingly including a deliberate error planted by the Japanese

research team who had actually done the work. " (Inventing the AIDS

Virus p.164). In 1984 Dr Gallo, presented the world HTLV-III, which

was renamed HIV later, and which became known as 'the AIDS virus' (See

Virus Myth).

 

A fundamental knowledge was necessary to be shown as the established

science from the days of Pasteur and the first vaccine against the

" work " of Dr. Gallo and the patents that he lodged to protect his test

kit.

 

In 1982, Robert Gallo from the National Cancer Institute in the USA,

put forward the hypothesis that the cause of AIDS is a retrovirus. One

year later, Myron Essex and his colleagues found that AIDS patients

had antibodies to the Human T-cell Leukemia virus Type-1 (HTLV-I), a

virus discovered by Gallo a few years earlier. At the same time, Gallo

and his colleagues reported the isolation of HTLV-I from AIDS patients

and advocated a role for this retrovirus in the pathogenesis of AIDS

(Emergency Medicine 1993;5:5-147: HAS GALLO PROVEN THE ROLE OF HIV IN

AIDS?, Eleni Papadopulos-Eleopulos, Valendar F. Turner, John M.

Papadimitriou). But there is no explanation why not all or a

statistically significant number of AIDS patients get leukemia which

is a natural expectation but instead get a host of opportunistic

infections including pneumonia and sarcomas.

 

The most difficult aspect of the HIV postulate is to have first

decided that their HIV virus is an aggressive pathogen which they

claim to target the immune system itself, as HIV was said to infect

the key CD4+ T cells that regulate the immune response, modifying or

destroying their ability to function and to reconcile this 'science'

with scientific data and evidence that some people " appear better able

than others to resist progression of HIV infection or developing

AIDS, " resulting in " long-term survivors " who can be divided into

three groups;-

 

1). Long-term nonprogressors who maintain healthy or steady levels

of CD4+ T cells despite many years of infection

 

2). Those tested HIV-positive individuals who lose a significant

proportion of CD4+ T cells but remain healthy, and

 

3). The people who remain uninfected despite repeated " exposure to

HIV " .

 

So, to save the HIV postulate for AIDS they also claim that, once the

virus infects CD4+ T cells, the virus' genetic material is permanently

integrated into the cell's chromosomes, establishing permanent latency

within infected cells. After infection, the HIV incorporates its

genetic material into the host cell DNA. If a cell reproduces itself,

each new cell also contains the integrated HIV genes. The virus can

hide its genetic material for prolonged periods until the cell is

activated and makes new viruses. So, its not an aggressive pathogen.

 

They also claim that other cells act as HIV reservoirs, harboring

intact viruses that may remain undetected by the immune system while

it " targets " the cells of the immune system.

 

There is also no explaination on how an infected cell remains normal

and remains undetected as an abnormal cell by NK cells or activated

macrophages after the HIV incorporates its genetic material into the

chromosomes of the cell. Such a virus, with such a capability, having

a sophisticated enzyme system to incorporate its genetic material into

the cells' chromosomes and activate it later on into replicating

itself cannot be so small and illusive that it avoids isolation and

replication by other virologists.

 

Virologist Dr Stefan Lanka states: " The rules demonstrating the

existence of HIV (and retroviruses in general) were never adhered to

by those who devised them nor were they ever validated. " A research

team at University of Western Australia claims that HIV has never been

isolated so far, and questions the existence of the virus-entity. So,

without a virus entity, how do you produce the test and offer it for

public use? Is this politics or science?

 

There are too many riddles to Dr. Gallo's virus. The Japanese research

team who had actually isolated viruses from some leukemia patients

including the deliberate error planted by them proves a lot of science

when taken together with the fact that most leukemia patients do not

have such a virus. Large amounts of viral toxins could create

oxidative stress on cells in the bones in persons who have low blood

antioxidant levels or these viral toxins could bind micronutrients in

these cells thereby shutting down the Krebs cycle and transforming

them into cancer cells that have switched to the alcohol energy

system. The antibodies produced could have destroyed the virus in the

blood and other fluids but not in the infected cells.

 

Selenium and Nitric Oxide

 

A similar stress on the Krebs cycle whether through viral toxins or

free radicals or a combination of both, suppresses it and consequently

cellular function and energy output are lowered causing the chronic

fatigue syndrome. Such a stress is more acute or chronic in

malnourished populations and would naturally be observed more

frequently in people with a low intake of selenium. Selenium is

essential for the production of selenium based enzymes in the body.

These enzymes are very important for mitochondrial metabolic activity

and for the prevention of mDNA depletion.

 

Exogenous free radicals and free radical generating chemicals and

pollutants, including from chemicals in cigarette smoke and very fine

pollutants in exhaust fumes can cause either an excess in the

production of endogenous NO or suppress its production. The body's

natural balance in the production of NO is perturbed. Too little

production diminishes NO required to scavenge ROS while excess NO is

known to cause cell and DNA damage and induction of cGMP. In the cell,

NO is capable of inducing iron depletion from iron stores, which in

turn is correlated with the activation of guanylate cyclase and

inhibition of mitochondrial respiration. NO has a great affnity for

iron and binds readily with iron-containing proteins such as

hemoglobin, myoglobin, cytochrome c, and guanylyl cyclase. NO

interacts with oxyhemoglobin to form methemoglobin and nitrate.

 

In excess, NO can inactivate mitochondrial electron transport and

ATPase. The role of oxygen reactive species in the depletion of NO and

the role of NO in iron biochemistry which in turn is critical in blood

cell formation in bones may provide the critical clue and link in the

formation of the leukemia cell under oxidative stress coupled with

imbalances in NO secretions in the body.

 

Chronic depletion of vitamin C in immune system cells also weakens the

immune system, particularly the macrophages and the NK cells that

secrete nitric oxide to destroy pathogens and cancer cells. Excess

nitric oxide acts as a free radical and destroys the biochemical

processes in bacteria and cancer cells but the large stores of vitamin

C in these cells protect them from their own excess secretions that

are in letal doses to cancer cells or invading bacteria. Hence,

ingestion of large amounts of bioavailable vitamins and minerals from

fruit juices and selenium intake would amount to a logical measure to

boost the natural antioxidant defense biochemistry as well as to boost

the health and optimal functioning of the immune system and in the

prevention of opportunistic infections. This is consistent with the

finding that the NK cell numbers fall with malnutrition, stress,

exercise, alcoholism, inadequate sleep, and in people with chronic

fatigue syndrome and other illnesses (Immune Response;). Immunotoxic

medication in persons with large amounts of viral toxins and/or free

radicals is a logical recipe to prevent recovery or hasten death or

diminish the quality of life.

 

If there is no virus that has been isolated and purified according to

accepted standards, what does the HIV test do? The proteins that are

used in the 'HIV' test are merely the biological outcome of stressed

white blood cells used in the lab and in 'Bio/Technology', June 1993,

'Aids' analyst, Dr Eleni Eleopulos exposed the non-specificity and

unreliability of the 'HIV' 'antibody test'.

 

The disclaimer on the packaging says it is not absolute proof that a

person tested positive has the virus that causes AIDS.

 

AIDS is acquired deficiency syndrome that can be acquired through

prolonged malnutrion or prolonged use of immunosuppressants. It

appears to fit more neatly into the free radical theory of AIDS or the

oxidative stress theory of AIDS, incuding its progression in the

individual and its " spread " in populations. Since there is a serious

doubt about a specific virus that targets the cells of the immune

system, when a person tests positive, it may be positive for an

antibody to a broken protein that is found floating as macrophage

debris, not yet filtered off in the spleen. Such protein particles may

be more commonly found in people recovering from another viral attack

such as flu or cold and in people recovering from parasitic infections

such as malaria.

 

Other conditions common in underprivileged and impoverished

communities that are known to cause false positive results are

tuberculosis, malaria, hepatitis and leprosy. False-positive ELISA

[antibody] test results can be caused by alloantibodies resulting from

transfusions, transplantation, or pregnancy, autoimmune disorders,

malignancies and alcoholic liver disease.

 

This can be interpreted as a positive reaction to antibodies that the

body may produce in other diseases or against other bodies that the

body's immune system may recognize as foreign but the final analysis

may just prove that it tests positive for a range of broken proteins

as a result of macrophage ingestion found floating in the blood and in

some white blood cells. That explains why they cannot be isolated and

purified and used to reinfect other cells in which they will replicate

like all other viruses.

 

Then there is the need to explain the antibodies which is a protective

immunological response to HIV infection. People with antibodies to HIV

should have protection against HIV disease, since vaccines protect by

inducing the production of antibodies. However, scientists found only

antibodies in HIV-positive patients, rather than the virus itself. And

having found the antibodies, the proponents of the HIV postulate want

the person with these antibodies to take a toxic poison like AZT and

other toxic retrovirals as medication rather than declare that he is

on the road to recovery like someone who has antibodies to the common

flu. This compounds the HIV riddle. Any normal and healthy person

taking them will probably die in 18 months and there is no record of

anyone with complete recovery after taking them.

 

This riddle is tightly linked with the official requirement to take

AZT and retrovirals after you are tested positive with antibodies

which is supposed to say that you now have an immune response and are

therefore safe - and that makes it bad. Yet, there are scientists at

official institutes working on government funds to develop the HIV

vaccine! So, when you test positive after being administered such a

vaccine and are found to test positive, off you go take retrovirals

and the AZT poison. Makes sense?

 

BELDEU SINGH

 

 

References:

 

Albrecht, E. W., C. A. Stegeman, et al. (2003). " Protective role of

endothelial nitric oxide synthase. " J Pathol 199(1): 8-17.

 

Nitric oxide is a versatile molecule, with its actions ranging from

haemodynamic regulation to anti-proliferative effects on vascular

smooth muscle cells. Nitric oxide is produced by the nitric oxide

synthases, endothelial NOS (eNOS), neural NOS (nNOS), and inducible

NOS (iNOS). Constitutively expressed eNOS produces low concentrations

of NO, which is necessary for a good endothelial function and

integrity. Endothelial derived NO is often seen as a protective agent

in a variety of diseases.

 

 

Anderson, T. J. (2003). " Nitric oxide, atherosclerosis and the

clinical relevance of endothelial dysfunction. " Heart Fail Rev 8(1):

71-86.

 

The endothelium plays a key role in vascular homeostasis through the

release of a variety of autocrine and paracrine substances, the best

characterized being nitric oxide. A healthy endothelium acts to

prevent atherosclerosis development and its complications through a

complex and favorable effect on vasomotion, platelet and leukocyte

adhesion and plaque stabilization. The assessment of endothelial

function in humans has generally involved the description of vasomotor

responses, but more widely includes physiological, biochemical and

genetic markers that characterize the interaction of the endothelium

with platelets, leukocytes and the coagulation system. Stable markers

of inflammation such as high sensitivity C-reactive protein are

indirect and potentially useful measures of endothelial function for

example. Attenuation of the effect of nitric oxide accounts for the

majority of what is described as endothelial dysfunction. This occurs

in response to atherosclerosis or its risk factors. Much remains to be

learned about the molecular and genetic pathophysiological mechanisms

of endothelial cell abnormalities. However, pharmacological

intervention with a growing list of medications can favorably modify

endothelial function, paralleling beneficial effects on cardiovascular

morbidity and mortality. In addition, several small studies have

provided tantalizing evidence that measures of endothelial health

might provide prognostic information about an individual patient's

risk of subsequent events. As such, the sum of this evidence makes the

clinical assessment of endothelial function an attractive surrogate

marker of atherosclerosis disease activity. The review will focus on

the role of nitric oxide in atherosclerosis and the clinical relevance

of these findings.

 

 

Ando, K. (2003). " [Oxidative stress]. " Nippon Rinsho 61(7): 1130-7.

 

Oxidative stress, which is enhanced in diabetes mellitus, causes

hypertension and plays a critical role on cardiovascular damages in

diabetes and hypertension. Angiotensin II is one of important

intrinsic oxidants in pathophysiology of hypertension. Reactive oxygen

species affect hypertension and its complications via inactivation of

nitric oxide, modification of lipid metabolism, and enhanced insulin

resistance. Moreover, oxidative stress and hypertension accelerate

cardiovascular damages. Thus, it is important to control oxidative

stress in hypertensive patients with diabetes.

 

 

Annuk, M., M. Zilmer, et al. (2003). " Endothelium-dependent

vasodilation and oxidative stress in chronic renal failure: impact on

cardiovascular disease. " Kidney Int Suppl(84): S50-3.

 

Despite significant progress in renal replacement therapy, the

mortality from cardiovascular disease (CVD) in patients with chronic

renal failure (CRF) is many times higher than in the general

population. The traditional risk factors are frequently present in CRF

patients. However, based upon conventional risk factor analysis, these

factors do not fully explain the extraordinary increase in morbidity

and mortality in CVD among patients with CRF. Accumulating evidence

suggests that CRF is associated with impaired endothelial cell

function. In recent years, the role of endothelial dysfunction (ED)

and excessive oxidative stress (OS) in the development of CVD has been

highlighted. ED is an early feature of vascular disease in different

diseases such diabetes, hypertension, hypercholesterolemia, and

coronary heart disease. The precise mechanism which induces ED is not

clear. Several factors however, including OS-related accumulation of

uremic toxins, hypertension and shear stress, dyslipidemia with

cytotoxic lipoprotein species such as small, dense low-density

lipoprotein (LDL) particles, competitive inhibition of endothelial

nitric oxide (NO) by increased production by asymmetrical

dimethylarginine (ADMA) are pathogenic. In addition, it is known that

excessive OS causes ED. An overproduction of reactive oxygen species

(ROS) may injure the endothelial cell membrane, inactivate NO, and

cause oxidation of an essential cofactor of nitric oxide synthase

(NOS). Recent studies have demonstrated that an impaired

endothelium-dependent vasodilation and OS are closely related to each

other in patients with CRF.

 

 

See also:

 

 

Harold Foster: What really causes AIDS?

 

Overcoming Aids, Infections, Heart Disease: Vitamin C Is Key

 

Harvard Research in Tanzania Confirms: Multivitamin Slows AIDS Progression

 

 

 

posted by Sepp Hasslberger on Tuesday October 11 2005