Reprinted from www.RobertoGiraldo.com, March 2004
Can "Co-Factors" Alone Cause AIDS?
By Roberto Giraldo, MD
“It has never been scientifically proven that HIV
destroys the immune system and causes AIDS. AIDS experts propose
a vast variety of "co-factors" that work together with
HIV in the genesis of AIDS. However, these "co-factors"
by themselves can generate AIDS with or without a positive HIV test
Since it has never been scientifically proven that HIV destroys
the immune system and causes AIDS (1), investigators who enthusiastically
defend HIV as the cause of the syndrome have proposed a vast variety
of agents as helpers or "co-factors" of HIV in the genesis
of AIDS (2,3). However, these "co-factors" are by themselves
causal agents of immunedeficiency and can generate AIDS with or
without the presence of a positive result on the antibody tests
for HIV (4,5). I do prefer to name the so-called "co-factors"
immunological stressor agents that can have chemical, physical,
biological, mental, and nutritional origin (6,7).
The following are some of the agents that have been proposed as
"co-factors" for HIV: alcohol, cocaine, heroine, morphine,
marihuana, cigarette smoking, amphetamines, volatile inhalants like
"poppers", environmental chemical pollutants, allergens,
CMV, herpes virus type 1, 2 & 6, herpes zoster, EBV, adenovirus,
retroviruses other than HIV, hepatitis A, B & C viruses, papovavirus,
mycoplasmas and other superantigens, tuberculosis, leprosy, malaria,
trypanosomiasis, filariasis, other tropical diseases, sexually transmitted
diseases, semen, blood, factor VIII, anxiety, depression, lack of
sleep and rest, exhaustible exercise, unsanitary conditions, poverty,
malnutrition and several vitamin deficiencies (2,3,8-11).
Let us see briefly how multiple, repeated and chronic exposure to
immunological stressor agents - "co-factors" - can degenerate
the immune system and cause AIDS:
1. ROLE OF CHEMICAL STRESSORS IN IMMUNODEFICIENCY
Practically every single medicament from the following groups have
been found to have immunotoxic properties: antibiotics; antifungal,
antiviral, and antiparasitic agents; tranquilizers, antiepileptics,
antiparkinson, and anesthetics; antihypertensive, anti-anginal,
and antiarrhythmic drugs; gastrointestinal medications; antidiabetics,
antithyroid drugs, and sex hormones including oral contraceptives;
antiallergics; bronchodilating agents; anticoagulants, drugs acting
on fibrinolysis, blood expanders, clotting factors, and inhibitors
of platelet aggregation; non-steroidal anti-inflammatory drugs,
corticosteroids, antirheumatismal, and anti gout drugs; and immunodepressive
and immunomodulating drugs such as antitumoral drugs and medications
to avoid graft rejection (12-14). The immunotoxicity of AZT has
been solidly documented (15-18).
Industrial chemical and environmental pollutants are another important
source of different abnormalities upon lymphocyte activation, proliferation
and differentiation, cytokine production, cytotoxic effect, antibody
production, phagocytosis, natural killer cell activity, complement,
etc., (19,20). Also here, immunotoxicity has been found in practically
every single chemical that has been tested from the following groups:
heavy metals, pesticides, aliphatic and aromatic hydrocarbons and
derivatives, alcohols, phenols, and derivatives, airborne pollutants
including diesel engine emissions, nitrogen dioxide, ozone, sulfuric
acid and food additives and preservatives (13,14,21).
The adverse effects of alcohol and other drugs on the immune system
have been documented since the beginning of last century (22). There
is a growing body of human and animal evidence of the immunotoxicity
of tobacco smoke, alcohol, marijuana, cocaine, heroine, alkyl nitrites,
met amphetamines, qualones and other street drugs (23-30). These
facts form some of the scientific bases for the "drug-AIDS
Chemical stressors can act as free radicals or stimulate the production
of them (33-35).
2. ROLE 0F PHYSICAL STRESSORS IN IMMUNODEFICIENCY
There is evidence that a variety of physical stressors lead to immunodeficiency.
Lymphocytes are much more radiosensitive than macrophages and plasma
cells, and alterations of the immune cells are in a dose-dependent
fashion. Radiation victims frequently succumb to infection (36,37).
Ultraviolet B radiation [UV] has often been implicated in local
and systemic immunosuppression (38). UV exposure decreases the counts
of total and helper T lymphocytes with inversion of T4/T8 ratio
(33). It also decreases plasma carotenoids, potent antioxidants
Exposures to other no ionizing radiations such as electromagnetic
fields, visible light, infrared, radio frequencies and microwaves,
lasers, very low and extremely low radiation frequencies have been
shown to increase the risk of degenerative diseases and certain
Vibration, heat, and high altitude stressors are also connected
to degenerative diseases in which the immune system is known to
play protective roles (45-46).
Free radicals have been clearly connected with physical stressors
and cell injury (33,35,47,48).
3. ROLE OF BIOLOGICAL STRESSORS IN IMMUNODEFICIENCY
The immunogenic properties of the components of human semen are
known to induce chronic stimulation of the immune system with subsequent
immunosuppression (49,50). Lymphocytotoxic autoimmunity is proposed
as a mechanism for this phenomenon (51). Passive anal intercourse
is recognized as a strong risk factor for AIDS (52-55), even for
HIV-negative individuals (47).
Blood and its components are known to be immunosuppresive (56).
It has been suggested many times that the immunological abnormalities
occurring in hemophiliacs are secondary to the immunogenic properties
of foreign proteins in the whole blood, in commercial clotting factor
VIII, or to the factor VIII itself (56-61). The hemophilia immunologic
dysfunctions are obviously proportional to the lifetime dose of
therapy received (61). Immunodeficiency has been described multiple
times in HIV-negative hemophiliacs (62,63). On the other hand, no
immunosuppression has been observed in hemophiliacs treated with
available purer factor VIII preparations (64). These facts are some
of the bases for "the foreign-protein-hemophilia AIDS hypothesis"
A prior requisite for any infectious agent to develop its potential
pathogenic properties is always host immunodeficiency (65). On the
other hand, and as a consequence of the host-infectious-agent relationships,
immunosuppression, especially of the cell-mediated immunity, occurs
during all infectious diseases (66). This is particularly valid
in intracellular infections [gonorrhea, listeriosis, legionellosis,
brucellosis, chlamydial infections, mycoplasma infections, rickettsial
infections, salmonellosis, tularemia, yersinia infections, and with
all viral diseases] (66,67). Immunodeficiency is also the rule during
infections with poly-immunogenic organisms leading to granuloma
formation, such as spirochetes [syphilis, bejel, yaws, pinta]; mycobacteries
[tuberculosis, leprosy]; fungi [dermatomycosis, sporotrichosis,
chromomycosis, histoplasmosis, blastomycosis, coccidioidomycosis,
paracoccidioidomycosis, cryptococosis, pneumocystosis, aspergillosis,
mucormycosis, candidiasis]; protozoa [toxoplasmosis, malaria, leishmaniasis,
trypanosomiasis, amoebiasis, giardiasis]; helminths [intestinal
helminthes, cysticercosis, hydatidosis, filariasis, schistosomiasis,
fluke infestations, toxocariasis] (66,68-71).
The role of parasites and infections as cause of immunosuppression
in the underdeveloped world has been addressed many times (8,10,11,72).
Reactive free radicals have been implicated in the generation of
immunodeficiency during the course of infectious diseases (73-75).
4. ROLE OF MENTAL STRESSORS IN IMMUNODEFICIENCY
Since the times of Galen [200 AD] it has been of public domain that
the mind can influence the body (76), particularly in disorders
related to immunity (77). Different immunological abnormalities
have been found in people under psychosocial stress (78). For example,
anxiety and depression decrease lymphocyte counts and functions
(79). Academic stress lowers natural killer cell activity, blastogenesis,
and interferon production (80). Bereavement decreases lymphocyte
proliferative response to mitogen and lowers natural killer cell
activity (81). DNA repair capability in lymphocytes is highly impaired
by mental distress (82).
Only in the last three decades have the intimate mechanisms that
allow mental stressors to cause immunodeficiency been clarified
Lymphocytes are known to produce all kinds of hormones and neurotransmitters,
originally known as being produced only by endocrine glands and
neurons (87,88). At the same time, lymphocytes have receptors for
all types of hormones and neurotransmitters, including endorphins
and encephalins (87). Neurons and cells from endocrine glands have
receptors for lymphokines (87). Therefore, brain, mind, endocrine
glands, and lymphoid tissues are biochemically interconnected (89)
to structure a critical part of our defense activities. Furthermore,
all types of stressors [chemical, physical, etc.,] share pathways
during any stress response to them (90).
The issue of mental stress as an immunodepressive agent has been
addressed many times in relation to the onset, course, and prognosis
of AIDS (78,91,92).
5. ROLE OF NUTRITIONAL STRESSORS IN IMMUNODEFICIENCY
The effects of malnutrition on lymphoid organs were first described
during the middle of 19th century (93). Lymphoid tissues are particularly
vulnerable to the damaging effects of malnutrition, and lymphoid
atrophy is a prominent feature in nutritional deprivation (94).
Cell division is a very singular characteristic of the functioning
of immunocompetent cells. All types of immune cells and their products,
such as interleukins, interferons, and complement, are known to
depend on metabolic pathways that employ various nutrients as critical
co-factors for their actions and activities (94). Most of the host
defense mechanisms are altered in protein-energy malnutrition [PEM],
as well as during deficiencies of trace elements and vitamins (95).
Patients with PEM have impaired delayed cutaneous hypersensitivity,
poor lymphocyte proliferation response to mitogens, lower synthesis
of lymphocyte DNA, reduced number of rosetting T lymphocytes, impaired
maturation of lymphocytes seen through an increased deoxynucleotidyl
transferasa activity, decreased serum thymic factor, fewer CD4+
cells, decreased CD4+/CD8+ ratio, impaired production of interferon
gamma and interleukin 2, altered complement activity [specially
reduction of C3, C5, factor B and total hemolytic activity], poor
secondary antibody response to certain antigens, reduced antibody
affinity, impaired secretory immunoglobulin A response, decreased
antibody affinity, and phagocyte dysfunction (94).
Human malnutrition is usually a composite syndrome of multiple nutrient
deficiencies. However, isolated micronutrient deficiencies do happen.
Vitamin A deficiency results in reduction in the weight of the thymus,
decreased lymphocyte proliferation, impaired natural killer cell
and macrophage activities, and increased bacterial adherence to
epithelial cells (96). Vitamin B6 deficiency produces failure of
several components of both cell-mediated and humoral immune responses
(94). Vitamin C deficiency impairs phagocytosis (97) and cell-mediated
immune reactions (102). Vitamin E deficiency also alters immune
responsiveness (94). Zinc deficiency generates lymphoid atrophy,
reduces lymphocyte responses and skin delayed hypersensitivity (94).
Copper and selenium deficiencies impair T and B lymphocyte functions
(94). Dietary deficiencies of selected amino acids such as glutamine
and arginine also alter immunity (94).
Intrauterine malnutrition causes prolonged, even permanent, depression
of immunity in offspring (98,99).
Considerable data implicate excess lipid intake in the impairment
of immune responses (100). The potential for free radical damage
is dependent in large part on the level of potentially oxidizable
fatty acids, mainly polyunsaturated fatty acids [PUFAs] in the diet
(33). High levels of dietary PUFAs have been shown to be immunodepressive.
Dietary fats may undergo free radical-mediated oxidation prior to
ingestion, as can occur when foods are fried (33. Animals fed oxidized
lipids show marked atrophy of the thymus and T lymphocyte dysfunctions
At molecular level, the damage to immunocompetent cells by several
nutritional deficiencies (Vitamin A, Vitamin C, Vitamin E, zinc,
copper, zelenium deficiencies) is caused by increased free radicals
through oxidative stress (94,102).
As Jain and Chandra (9) have found, "...there is an uncanny
similarity between the immunological findings in nutritional deficiencies
and those seen in AIDS". The role of nutritional stressors
in AIDS has been addressed many times (103,104).
6. ROLE OF FREE RADICALS IN IMMUNODEFICIENCY
Free radical reactions of special significance to immunological
phenomena are, for example, many oxidizing agents that can abstract
a hydrogen atom from thiol groups to form thiyl radicals. Thiol
groups are important for enzyme activities, receptor functions,
disulphite links in immunoglobulins, and T cell activation and proliferation
(105). The super oxide anion radical can react with nitric oxide
resulting in loss of endothelium-derived relaxing factor activity
(106), which is important in the inflammation/ disinflammation process.
Methionine oxidation can cause protein damage with subsequent changes
in immunogenicity (107). Proteolysis can be increased by free radical
damage (108). The per oxidation of lipids by reactive free radicals
produce many biological modulators as for example the 4-hydroxy-alkelans
which produces strong chemotactic activity for phagocytes (109),
alters the adenyl cyclasa system, increases capillary permeability,
and alters lymphocyte activation (110). Lipid hydroperoxides, also
from per oxidation of lipids, alter lymphocyte activation (110).
Conditions favoring lipid per oxidation may result in chemo taxis
of leukocytes, protein modification, immune complex injury, and
cell death (105).
Free radicals are produced over the regular immune system network.
Despite the beneficial effects of the inflammation responses, they
can also aggravate existing tissue damage by releasing free radicals.
When uncontrolled, initiated by an abnormal stimulus, or occurring
for prolonged periods of time, inflammation may become the disease
process (111). It is critical for optimal immune responses that
there be a balance between free radical generation and antioxidant
protection (33). During phagocytosis by polymorphonuclear leukocytes
for example, super oxide anion radicals are released (112). These
oxygen free radicals can oxidize thiol groups to thiol radicals,
and can stimulate lipid per oxidation with the formation of H2O2,
which is very significant in the mechanisms of cell injury (105).
Oxygen free radicals produced during phagocytosis of immune complexes
are associated with the injury due to immune complexes (113).
It has been proposed several times that free radicals and specifically
oxidizing species play important roles in the pathogenesis of AIDS
I propose that at a physiological level, AIDS can be explained as
a progressive degenerative alteration of different immune cells
and immune metabolic reactions, secondary to multiple, repeated,
and chronic exposures to immunological stressors. This degeneration
can be caused by an immunotoxic effect of stressors on immunocompetent
cells. Also, it can be the result of over stimulation/activation
of the immune cells through an immunogenic effect. Many chemical
and biological stressors can have an immunogenic effect on the immune
cells and functions. Additionally, physical, mental, nutritional,
and, again, chemical stressors can have an immunotoxic effect on
the same cells and activities (4,5).
At a molecular level, AIDS is the result of alterations of immunocompetent
cells and immune metabolic reactions due to an excess of free radicals
especially oxidizing agents. Eleni Papadopulos-Eleopulos has proposed
elegantly the role of oxidizing agents in the pathogenesis of AIDS
since 1988 (119).
AIDS is neither an infectious disease nor is sexually transmitted.
It is a toxic/nutritional syndrome caused by the alarming worldwide
increment in immunological stressor agents.
8. TRIAL PROPOSAL
I propose the following experiments to find out the real role of
immunological stressors - co-factors - in the causation of AIDS:
To have three groups of people: a) symptomatic AIDS patients, b)
HIV-positive asymptomatic individuals, and c) very healthy HIV-negative
The AIDS patients as well as the HIV-positive asymptomatic groups,
may have individuals from all the groups at risk for AIDS: drug
addicted and non-drug addicted gay males, IV and non-IV drug addicted
individuals, prostitutes, hemophiliacs, blacks and Hispanics in
USA, Africans and Asians, children from developed and underdeveloped
countries, AIDS-phobic people, and an occupational group. The normal
individuals to be used as controls may match as much as possible
with the individuals in the other two groups.
Retrospective trial. Before starting any treatment to check in the
three groups for:
- Exposure to immunological stressors of chemical, physical, biological,
mental, and nutritional origin. Using a questionnaire to check retrospectively
for past exposures to chemical, physical, biological, mental, and
nutritional immunological stressors.
- Levels of oxidizing agents. To check in all of them for the presence
and levels of surrogate markers of oxidation.
- "HIV status" To run on all individuals of the three
groups ELISA, Western blot and PCR tests.
- Immune system response capabilities. Besides counting all the
T and B cell subsets, it is necessary to evaluate the functioning
status of lymphocytes, as well as all other immunocompetent cells,
by tests such as lymphoblastotransformation, inhibition of migration,
lymphocyte activation etc. To check the levels of all components
of the complement system. To check electrophoresis of proteins,
immunoelectrophoresis, levels of serum immunoglobulins G, A, M,
D, and E; to check for the presence of all type of autoantibodies;
circulatory immune complexes; and skin test reactions. Beta 2 microglobulin
- Physiological status of all other systems. To rum complete chemical,
hematological, urine and stool profiles. Also to check the status
of the endocrine glands, liver, and kidneys. To find out levels
of micronutrients such as B-complex vitamins, Vitamin C, betacarothene,
vitamin E, selenium, zinc, magnesium, etc. Beta 2 microglobulin.
Prospective trial. To follow up the three groups for several years
with periodical clinical and laboratory evaluation.
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