Introduction

 In the  last two years, I reviewed the medical records of several individuals (male and female) who were diagnosed with idiopathic illnesses  of the nervous system, respiratory system, kidneys, and  liver or asthma. They  were treated chronically with glucocorticoids or with glucocorticoids and cytotoxic  drugs at moderate to high therapeutic doses. These people lived in different  states within  the United States. They consulted with me to find out if their  exposure to chemicals at the workplace and/or the use of medications triggered  and/or contributed to their illnesses. The  review of their medical files showed  that all of them suffered from various degrees of lymphocytopenia.  One of these  cases was a 60 year-old-white male who developed Immunodeficiency syndrome  similar  to those described in patients with Acquired Immune Deficiency Syndrome (AIDS)  and Idiopathic CD4+ T cells lymphocytopenia (ICL)¹ after treatment  with a two months course  of prednisone (60 mg per day) and two weeks course  of azathioprine (50-100 mg per day) for lung fibrosis. His blood analysis revealed  a CD4+ T cells count of 255/µL (normal range  542 to 1595/µL) and a CD4+T cells  /CD8+ T cells ratio of 0.6 (normal range 1.0-3.5). He was suffering from a severe  lymphocytopenia (peripheral blood lymphocytes count was 483/µL).  Prior to his  treatment with prednisone, his lymphocytes count was normal (1513/µL). In addition,  he suffered from pneumonia and developed a severe fungal infection on the skin  of various regions  of his body and very painful sores in his mouth (gum and  cheeks which looked like white cottage cheese). He was not infected with the  Human Immune Deficiency Virus (HIV) as determined by three  tests at various  clinics.

This  man was diagnosed as having Idiopathic Pulmonary Fibrosis (IPF) in June of 1997  at Kaiser Permanente Medical Center in  Vallejo, California. My review of the  work history of this man revealed that he had been working at Travis Air Force  Base in Fairfield, California since 1979 as a flight engineer. He had been  exposed  chronically at his workplace to organic solvents and aviation jet fuels (JP-8  in particular which is composed of 99% kerosene²). The review of  his medical records revealed that he had  pulmonary fibrosis and changes in the  upper respiratory airways (hyperplasia and metaplasia of the epithelial layers  and hyperplasia of the smooth muscle cells) that were consistent with  the changes  resulting from long term exposure to toxic levels of kerosene and aviation fuel  by inhalation.^3-7

The  treating physician at Kaiser Permanente changed the course  of treatment for  this man in November of 1997 based on the diagnosis and the recommendation that  I provided. He showed significant improvements in his general health condition  and in his  immune system. His physician stopped the treatment with azathioprine,  tapered the treatment with prednisone and treated the patient with anitihistamine  (Chlorpheninamine, 24 mg/day) to  relax the muscle of the airways. On May 19,  1998, 22 days after the last dose of prednisone, his CD4+ T cells and CD8+ T  cells counts were 657 cells/µL and 659 cells/µL, respectively. These  counts  were 247% and 153% of the values during the tapering of prednisone for the CD4+  T cells (T4) and the CD8+ T cells (T8), respectively. In addition, his fungal  infection and pneumonia were  resolved following treatment with short course  of antibiotic (Doxycycline 200mg per day for 2 weeks) and topical antifungal  agent (Loprox). In June of 1998, this man was treated with  colchicine (0.6-1.2  mg/daily) for two weeks for a minor joint problem. On September 30, 1998, his  CD4+ T cells count was 516/µL, 21% lower than the count on May 19, 1998 prior  to  treatment with colchicine. It took four more months to bring CD4+ T cells  count to 719/µL. It is clear that prednisone, azathioprine and colchicine were  all responsible for lowering CD4+ T cells in this patient.

The  striking similarity between the immunodeficiency syndrome observed in this case  and those described by Fauci et al.and Galloin patients  with AIDS and ICL, combined with the wide use of  immunosuppressive agents in  modern medicinal practice to treat a variety of chronic illnesses (thrombocytopenia,  pulmonary fibrosis, chronic joints disease, peripheral neuropathy, etc.) gave  me the  incentive to review the medical literature to evaluate the HIV-hypothesis  and the contribution of the illicit drugs, alcohol, and therapeutic agents,  and malnutrition to the pathogenesis of AIDS.^1,8-11

The  HIV-hypothesis states that HIV cause AIDS by killing the CD4+ T cells directly  or indirectly and after long incubation times (about 10 years), the number of  these cells will reach very low  levels which lead to severe immune deficiency.  Patients with severe immune deficiency (CD4+ T cells < 200/µL) usually suffer  from opportunistic infections (viral, bacterial, fungal, yeast, and/or  parasitic)  and certain form of cancer such Kaposi's sarcoma and lymphoma. It follows that  treatment of patients with antiviral drugs such inhibitors of reverse trascriptase  (AZT) or protease  inhibitors can delay the progression of AIDS by preventing  HIV replication in the cells.^1,8

My initial review of the medical literature revealed that the short  and the long term use of glucocorticoids at therapeutic doses, resulted independently of HIV in a variety of effects on the immune system that range from a transient reduction in T cells count in  peripheral blood to the development of full blown AIDS.^1,9,12-29 Table 1 contains a list of the wide range effects of glucocorticoids on the immune system, respiratory system, and other tissues.

 Kaposi's  sarcoma (KS) can develop in patients chronically treated with glucocorticoids  independently of HIV. For example, KS developed eight months after initiation  of prednisone treatment  (40 mg per day for three months) in a 58-year-old man  with systemic rheumatoid disease.³⁰ He also had lymphocytopenia (896/µL),  reduction of T4 cells (215/µL ), and T4/ T8 ratio of 0.7.  This man was HIV-negative  as tested by western blot. In addition, there are many cases who developed KS  following treatment with glucocorticoids. They had reversal of their lesions  after the  termination of the treatment. Table 2 contains a brief description  of 16 such cases.

The  reversal of CD4+ T cells depletion in the peripheral blood was  also reported  in HIV+ homosexual men after the termination of their treatment with glucocorticoids  (Table 2). Sharpstone et al., reported that eight HIV+ males with inflammatory  bowel disease  who used rectal steroid preparation had a decline in their CD4+  T cells at a rate of 85 cells/µL per year. Four of them underwent colectomy  that eliminated the need for the steroid and their CD4+  T cells increased 4  cells/µL per year. Eight case-matched controls who did not have surgery continued  to have a decline of 47 cells/µL per year.³¹ This shows the importance  of measuring CD4+  T and CD8+ T cells in patients chronically treated with moderate  or high therapeutic doses of glucocorticoids.

Nineteen years have passed since the first cases of AIDS were  reported in the United States, and the leaders of the HIV-hypothesis   still are uncertain about the pathogenesis of AIDS.³²  They continue to contradict each other on the ways that  HIV is purported to destroy CD4+ T cells. In 1987, Robert Gallo   stated that "many T4 cells are infected in the lymph node during contact with a macrophage. After a variable latency, the infected  lymphocyte may be killed by viral replication. Clearly the T4 population is reduced by the death of infected cells".⁸  In 1998, Fauci et al. stated that "apoptosis is strictly dependent on cellular  activation. Direct infection of CD4+ T cells with HIV is not required for apoptosis to occur".  They also stated that "it is difficult to explain completely the profound immunodeficiency noted in  HIV-infected individuals solely on the basis of direct infection and quantitative depletion of CD4+ T cells".¹

I  have found no scientific evidence to indicate that HIV can kill  infected T4  cells (CD4+ T cells) in vitro or in vivo. In addition, the abnormalities  in the immune system of patients with AIDS are not restricted to the reduction  of T4 cells as predicted by the  HIV-hypothesis.^1,8 In 1985, Hoxie  et al. observed no evidence of death in T cells infected with HIV in tissue  culture. These cells continued to produce virus particles for more than four  months  after inoculation with the virus.³³ I reviewed many reports  describing the changes in the lymph nodes of patients infected with HIV and  have found that the changes range from extensive  cellular hyperplasia of T and  B lymphocytes and the supporting stroma to severe atrophy of the glands.^34-42 Table 3 lists the changes in the lymph nodes of 505 HIV infected patients who   were asymptomatic or had AIDS. Three distinct stages of changes in lymph nodes  are evident. These are hyperplasia (245 patients), atrophy (117 patients), and  mixed stage (172 patients). The  presence of hyperplasia in the infected lymph  nodes contradicts the HIV-hypothesis that states that HIV destroys infected  T cells.^1,8

 My  conclusions are also supported by the findings reported by the leaders of the  HIV-hypothesis. In 1995, Muro-Cacho, Pantaleo, and, Fauci examined 29 HIV+ lymph  nodes and found twelve of  these lymph nodes with follicular hyperplasia and  extensive germinal centers, five with follicular hyperplasia mixed with follicular  involution, twelve lymph nodes with a mixture of  follicular involution and lymphocyte  depletion, and five lymph nodes with lymphocyte depletion. They stated that  "apoptosis was not restricted only to CD4+ T cells; both B cells and CD8+  T cells  were found to undergo apoptosis. Taken together, these results indicate  that the increased intensity of the apoptotic phenomenon in HIV infection is  caused by the general state of immune  activation, and is independent of the  progression of HIV disease and the levels of viral load".⁴² HIV provirus was also found in CD4+ T cells, CD8+ T cells, and B cells lymphocytes  in the lymph nodes  of HIV infected patients⁴³ and its ability to  infect cells is not restricted to cells that have CD4 receptor as predicted  by the HIV-hypothesis.^1,8

 Furthermore,  in Tanzania, Fawzi et al. studied the influence of multivitamin supplements  in the diet on T cells counts in peripheral blood in 1,075 HIV infected pregnant  women who had  poor nutritional status. These women received regular diet (n=267),  vitamin A (n=269), multivitamins excluding vitamin A (n=269), or multivitamins  including vitamin A (n=270) in a  randomized, double-blind, placebo-controlled  trial between 12 and 27 weeks of gestation. The T cells (CD4+ , CD8+, and CD3+)  increased in all groups between baseline (mean =18 weeks  gestation) and 6 weeks  postpartum. The average CD4+ T cells at baseline were 423 and 424/µL for the  placebo and multivitamins group, respectively. At 6 weeks postpartum, the average  CD4+ T  cells count were 520/µL (123% of baseline) for the placebo and 596/µL  (141% of baseline) for the multivitamins group.⁴⁴ This large study  showed very clearly that not only is there is no killing  of T cells by HIV in  vivo, but on the contrary, significant increases of T cells had occurred  for 20 weeks in the presence of HIV. These findings are also supported by the  observation of the leaders of  the HIV-hypothesis. Fauci et al. reported that  there are thousands of HIV+ individuals living in the United Stated of America  without any health problem since their infection with HIV approximately ten   years previously. They estimated their number to be about 5% of the HIV infected  cases in USA (28,690 individuals as of 1/1/1997). They labeled these unexplained  HIV+ healthy individuals, "  long-term nonprogressors."¹

My  investigation also revealed an astonishing result: the majority of AIDS patients  who participated in the four major Zidovudine  (AZT) clinical trials were HIV-negative  prior to their treatment with AZT.^45-8 These studies cumulated in  the approval of AZT by the USA FDA to treat AIDS and aymptomatic HIV+ patients.  Therefore,  it is sadly ironic that the conclusions of these studies stating  that AZT prolongs the lives of patients with AIDS or prevents the development  of AIDS in asymptomatic HIV infected individuals are  false. Briefly, a total  of 2,349 patients participated in these studies, and at least 77% of them were  HIV-negative prior to their treatment with AZT. HIV status of participants upon  entrance to  these studies are: 1) Fischl et al., 1987: 282 patients participated;  HIV was isolated at entry from 160 patients (57 percent of the AZT group and  58 percent of the placebo group); 2) Fischl et al., 1990:  406 AIDS patients  were treated with AZT but only 50 percent of these subjects had detectable serum  levels of HIV antigen before treatment; 3) Volberding et al., 1990: 1338 subjects  participated;  only 117 patients (9%) had detectable levels of HIV p24 antigen  at baseline; and 4) Hamilton et al., 1992: 321 AIDS patients received AZT but  only 63 patients (20%) had detectable level of  p24 antigen at base-line. The  findings of these studies clearly demonstrate that AIDS in 77% of these patients  was caused by agent(s) or processes other than HIV. Moreover, the treatment  of  very sick people with a very toxic drug, AZT was not beneficial.

Fauci  et al. stated, "in 1983, human immunodeficiency virus (HIV) was isolated  from a patient with lymphadenopathy, and by 1984 it  was demonstrated clearly  to be the causative agent of AIDS". ^1(p.1791) My review of the  literature did not lead to any medical facts that link HIV as the cause of AIDS.  It did reveal that  approximately 90% of AIDS cases in the USA and Europe are  observed in homosexual men and drug users.^1,49,50 The regular uses  of alcohol, heroin, cocaine, amphetamines, and alkyl nitrite  cause chronic health  problems of the nervous system, respiratory system, cardiovascular system, kidneys  and other tissues in these individuals. The majority of these health problems  are usually  diagnosed as idiopathic currently, and treated with high doses of  glucocorticoids and/or cytotoxic drugs.^{1,9-11, 32,51-93} Homosexual  men are usually heavy user of illicit drugs, alcohol, and rectal  glucocorticoids.^1,49,50 The treatment of a patient with prednisone at 60 mg per day for about three  months can actually cause AIDS as described above. This dose is usually given  to patients  suffering from lung fibrosis, thrombocytopenia, and other chemically  induced chronic illnessess.¹

The  medical evidence described above indicated that the  HIV-hypothesis ignores many  crucial pieces of evidence that are important in the pathogenesis of AIDS, the  programs designed to treat the patients with AIDS, and to solve the AIDS crisis.  P. H.  Duesberg also came to the same conclusionin 1987.^49,50 He has challenged the HIV-hypotheses since 1987 and has presented overwhelming  evidence in his publications indicating that the use  of the illicit drugs and  alcohol by the risk groups may have important roles in the pathogenesis of AIDS  in America and Europe and should be evaluated.

 For  these reasons, I reviewed more than one thousand published articles and several  standard medical text books in many medical subjects (pathology, toxicology,  pharmacology, immunology,  nutrition, endocrinology, infectious diseases, and  human medicine) to evaluate the role of drugs, malnutrition, and infectious  agents in the pathogenesis of AIDS. My goals were to pin-point the causes  of  AIDS, to explain the pathogenesis of the AIDS syndrome, and, hopefully, to suggest  an appropriate approach to cure this disease. I am very happy to state that  my major objectives have  been achieved. The next sections contain detailed description  of the pathogenesis of AIDS in America, Europe, Africa, and other countries  for all risk groups. It also contains a list of  recommendations for treating  patients with AIDS and preventing the occurrence of AIDS in patients within  each risk group.

Tables  1-3 (Pages 8-13)

 Table 1. Acute  and chronic toxicity of glucocorticoids and their contribution  to the pathogenesis of AIDS

Table 2. Cases  of Kaposi's sarcoma and CD4+ T cells  lymphocytopenia induced by the  treatment of immunosuppressive drugs and reversed  by termination of the treatment

Table 3. Histopathologic  changes in lymph nodes of HIV + drug  users, homosexuals,  and hemophiliacs with persistent nonmalignant  lymphadenopathies

Explanation of the  information presented in Table 1

• The  information presented in this Table shows the acute and chronic effects of  glucocorticoids on the functions of the immune system and other several vital  organs and tissues.  Glucocorticoids reduce the functions and the numbers of  T and B cells lymphocytes and macrophages. They cause adrenal insufficiency  and interfere with growth of bone, muscle, and  other peripheral tissues and  delays wound healing. The chronic use of glucocorticoids cause atrophy of  the lymph nodes and increase the incidence of infections by opportunistic   pathogens. They also increase the incidence of cancer. All lesions and the  symptoms described in this Table were observed in patients with AIDS (weather  HIV+ or  HIV-negative) and people suffering from severe malnutrition (weather  HIV+ or HIV-negative). Malnutrition induces the release of endogenous cortisol  that acts similarly to therapeutic corticocorticoids.
   
• Glucocorticoids  are widely used currently in modern medicinal practices to treat many acute  and chronic health conditions that result from the use of illicit drugs and  alcohol such as  thrombocytopenia, pulmonary fibrosis, peripheral neuropathy,  tuberculosis, etc. Rectal corticosteroids are also widely and chronically  used by homosexual men to treated wide range of  chronic rectal and gastrointestinal  diseases that result from practicing anal sex. Hemophiliacs are also use glucocorticoids  and other immunosuppressive agents to prevent the  development of inhibitors  for factors VIII and IX and to treat chronic joint illness. Patients receiving  blood transfusions and/or transplanted tissues also use glucocorticoids to   prevent anaphylactic reactions and tissue rejection.
   
• Glucocorticoids  are also used to treat respiratory illness and other illnesses in premature  babies. The use of cocaine and other illicit drugs during pregnancy increases  the incidence of premature delivery.
   
• Glucocorticoids  are used by all risk groups prior and after their diagnosis with AIDS. Glucocorticoids  cause the symptoms and lesions that are observed in patients with AIDS, not  the HIV.

Table  1. Acute and chronic toxicity of glucocorticoids and their contribution  to the pathogenesis of AIDS

 

Target cells, organs,and processes Effects1,9,12-29 Lymph nodes Atrophy (fibrosis and fatty degeneration)17 Lymphocytes (B and T cells) 01,9,12-16 Decrease numbers in circulation (B and T cells).Alters  the migration patterns of lymphocytes. Suppress cutaneous delayed-type hypersensitivity   reaction to antigens and reduces expression of lymphocyte function. Decrease  lymphoid cell access to antigens in inflammatory sites and antigen blastogenesis. B cells1 Increase the incidence of lymphoma Monocyte and Macrophages1,9,15,16  Reduce their release from bone marrow and  their numbers in circulation. Reduce endocytosis and reticuloendothelial  system clearance. Decrease  bactericidal and fungicidal clearance. Reduce  effects of mediators on macrophage. Leukocyte Cause leukocytosis.1,9 Adrenal glands  Cause secondary adrenal insufficiency.1,9 Respiratory system Inhalation of glucocorticoids aerosol (Beclovet)  increases infections with Candida albicans and/or Aspergillus niger in the  mouth and pharynx and  occasionally in the larynx. Positive culture for oral  Candida may be present in up to 75% of patients.9 Wound healing Both systemic and topical glucocorticoids cause  a variety of skin changes, including acne-form eruptions, atrophy, striae.  High doses can retard  wound healing and increases the risk for bacterial,  yeast, and fungal skin infection.1,9 Mesenchyma Increase the incidence of Kaposi's sarcoma.1,9,17-29 Activation of infectious Increase the incidence of viral, bacterial,  fungal, and parasitic infection.1,9 Muscle and Bone Myopaties and bone disorders.1

Table  2. Cases of Kaposi's sarcoma and CD4+ T cells lymphocytopenia  induced by the treatment of immunosuppressive  drugs and reversed by termination  of the treatment

Condition Number of Patients AIDS Indicator Description of 32 Cases 18-29,31 HIV+/16 Reduction of CD4+T cells Eight HIV+ males with inflammatory bowel disease  who used rectal steroid preparations had a decline in their CD4+ T cells  to 85 cells/µL per year.  Four of them underwent colectomy that eliminated  the need for the steroid and their CD4+ T cells increased 4 cells/µL per  year. Eight case matched controls had a decline of 47 cells/per year.31 KS/8   Eight patients developed KS after treatment  with a steroid for chronic illness. The lesions regressed after the cessation  of treatment. 18-25 HIV-negati ve KS/8   Eight organ transplant patients developed KS  after treatment with cyclosporin and prednisone. Their lesions regressed  after the cessation or  reduction of the treatments .26-29

Explanation  of the information presented in Table 3

• The information  presented in this Table describing the pathology of the lymph nodes in HIV  infected individuals who are asymptomatic or with AIDS. This medical evidence  shows  the following facts that disapprove the claims of the HIV- hypothesis  that HIV is the cause of AIDS.
• HIV  was isolated from lymph nodes showing cellular hyperplasia (T and B cells  ) and this fact contradicts the claim of the HIV-hypothesis that HIV kills  CD4+ T cells.
• HIV  was isolated from lymph nodes showing severe atrophy (reduction in lymphocytes  and stroma) and this contradicts the claim of the HIV- hypothesis that the  HIV causes  selective T cells necrosis. It is believed that HIV kills only  CD4+ T cells because these cells have CD4 receptor that binds with HIV protein.  Actually, this type of atrophy in the  lymphoid organs is usually associated  with chronic use of glucocorticoids and/or severe malnutrition.
• The  information shows that the disease passes through three stages in the lymphoid  tissues. These are hyperplasia, mixed phase (hyperplasia and atrophy), and  atrophy. The symptoms  of AIDS are usually associated with development of atrophy.

Table  3. Histopathologic changes in lymph nodes of HIV+ drug users, homosexuals, and hemophiliacs with persistent nonmalignant  lymphadenopathies

Lesions Type Description of changes in lymph nodes of 505  patients34-42 Number of Patients (A) Follicular hyperplasia34-42 Hyperplastic germinal center. Cellular regeneration  with much mitosis. Hyperplasia of the T zone CD4+ T cells > CD8+ T cells.  Immature sinus  histocytosis. Extensive cytolysis and phagocytosis. Scattered  Multinucleated giant cells. Clusters of polymorphonuclear neutrophils. Multifocal  hemorrhage. 245 (B) Mixed type34-6,39-41 Lesions are mixed between A and C 172 C) Follicular Involution34-7,39- 41 Lymph nodes with atrophic burnt-out follicles.  Follicles are small and are depleted of lymphocytes. CD8+ T cells > CD4+  T cells. Follicles are  inconspicuous and focally hyalinized. Loss of lymphocytes  from interfollicular cortex. Extensive diffuse vascular proliferation. Depletion  of dendritic cells. Thickened capsule. 117