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 glucocorticoids aerosol by the US 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  antiviral 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 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 presence of hyperplasia in the infected lymph nodes contradicts the HIV-hypothesis which states HIV destroys infected T cells (Gallo, 1987;  Fauci et al., 1998)

Further elucidation is provided by the proponents  of the HIV-hypothesis.  Muro-Cacho, Pantaleo, and, Fauci  (1995) 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 activities and the levels of viral load”.  HIV provirus was also found in CD4+ T cells, CD8+ T cells, and B cells lymphocytes in the lymph nodes of HIV infected patients and its ability to infect cells is not restricted to cells that have  CD4 receptor as predicted by the HIV-hypothesis (Al-Bayati, 1999).

The changes in the lymph nodes described above are not unique to HIV infected individuals but also were described in HIV-negative patients in risk groups. The lymph nodes from 215 HIV-negative homosexual and drug users men showed hyperplasia and atrophy and 15 lymph nodes 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).

In addition to the information presented above that demonstrate the invalidity of the HIV-hypothesis, the rate of T cells infection by HIV, and the rate of the thymus and the lymphoid tissue regeneration also conflict with the HIV-hypothesis.

Next: HIV cannot kill enough t-cells

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