Causes and pathogenesis of AIDS in drug users and homosexuals

Causes and pathogenesis of AIDS in drug users and homosexuals

The appearance of AIDS in the USA and Europe in drug users and homosexuals in the late 1970s and early 1980s coincided with the synergistic actions of several events. Briefly, these include the spread of illicit drug use, especially smoking crack cocaine and heroin in 1970s, the approval of aerosols containing glucocorticoids by the U.S. FDA in 1976, the wide use of the glucocorticoid inhalers to treat chronic respiratory illnesses resulting from inhaling cocaine and heroin, the wide use of alkyl nitrites by homosexuals to facilitate anal sex in 1970s, and the wide use of corticosteroids to treat chronic gastrointestinal tract illness in homosexuals. Furthermore, the approval of anti-retroviral drugs (AZT and protease inhibitors) and the steroids by the U.S. FDA to treat patients with AIDS and asymptomatic patients infected with HIV has exacerbated the problem (Al-Bayati, 1999).

The HIV hypothesis states that HIV causes AIDS by killing the CD4+ T-cells directly or indirectly (Fauci, et al., 1998). It appears that there is no scientific evidence to show 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. Hoxie et al. (1985) 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. Many reports describe the changes in the lymph nodes of patients infected with HIV and these changes range from extensive cellular hyperplasia (excessive production) of T and B lymphocytes and the supporting stroma to severe atrophy of the glands. Changes in the lymph nodes of 505 HIV- infected patients who were asymptomatic or had AIDS demonstrate three distinct stages. These are hyperplasia (245 patients), atrophy (117 patients), and mixed stage (172 patients) (Al-Bayati, 1999). The occurrence of hyperplasia in the infected lymph nodes contradicts the HIV hypothesis which states that HIV destroys infected T-cells (Gallo, 1987; Fauci et al., 1998).

The changes in the lymph nodes described above are not unique to HIV-infected individuals, but have also been found in HIV-negative patients in risk groups. The lymph nodes of 215 HIV-negative homosexual men who were drug users showed hyperplasia and atrophy, and lymph nodes of 15 men showed Kaposis sarcoma and lymphoma. These changes are AIDS-indicator diseases based on the CDCs criteria, yet the subjects were HIV-negative (Al-Bayati, 1999).

Duesberg, (1992) stated that HIV infects on the average only 0.1% (1 out of 500 to 3000) of T-cells in AIDS patients, and at least 3% of all T-cells are regenerated during the two days it takes a retrovirus to infect a cell. HIV could never kill enough T-cells to cause immunodeficiency. Thus, even if HIV killed every infected T-cell, it could deplete T-cells only at 1/30 of their normal rate of regeneration, not considering activated regeneration. The study by me and my colleagues (Al-Bayati et al. 1990) also showed that the rate of regeneration in the damaged thymus and lymphoid tissue of mice treated with a lymphotoxic agent (vanadate) was very rapid.

In addition to illicit drug and alcohol abuse, some homosexuals are also heavy users of alkyl nitrites that relax the anal muscle and facilitate anal sex. It has been stated that the use of alkyl nitrites permeated the gay life by 1977 (Al-Bayati, 1999).

Some homosexuals usually suffer from acute and chronic rectal and gastrointestinal diseases that dictate the heavy therapeutic use of rectal steroids. Among 7 selected studies that included 736 patients who were infected with HIV and/or had AIDS, 97% were homosexual or bisexual men. They show clearly that homosexual men suffer from extensive rectal and gastrointestinal problems that result in chronic use of therapeutic rectal steroids (Al-Bayati, 1999).

Review of the medical literature revealed that the short and the long term use of glucocorticoids at therapeutic doses, resulted 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. Since the harmful effect of corticosteroids is broad, it is not surprising that many types of infections seem to occur more often in patients treated with corticosteroids.

In addition, Kaposis sarcoma (KS) can develop, independently of HIV, in patients chronically treated with glucocorticoids. Many cases, which developed KS following treatment with glucocorticoids, had reversal of their lesions after the termination of the treatment (Al-Bayati, 1999).

The high prevalence of adrenal insufficiency among AIDS patients provides very strong evidence that AIDS in these patients is caused by the use of corticosteroids. The most common abnormality seen in HIV-infected individuals is hyponatremia, which is found in up to 30 percent of patients. Scientists have also stated that the presence of a low sodium level, combined with a high serum potassium level, in a patient should alert one to the possibility of adrenal insufficiency and adrenocortical insufficiency as seen following prolonged administration of excess glucocorticoids.

Furthermore, as stated above, that the CD4+ T-cells depletion in the peripheral blood of HIV-positive homosexual men was reversed after the termination of their treatment with glucocorticoids, and at least 77% of 2349 patients who participated in the four major AZT clinical trials (1987-1992) were HIV-negative prior to their treatment with AZT. These studies demonstrate clearly that HIV is not the cause of AIDS (Al-Bayati, 1999).