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The Relationship between AIDS and HIV

June 7, 2000

Immunologic Profile of People with AIDS

It is well established that a number of viral, rickettsial, fungal, protozoal and bacterial infections can cause transient T cell decreases (Chandra, 1983). Immune deficiencies due to tumors, autoimmune diseases, rare congenital disorders, chemotherapy and other factors have been shown to render certain individuals susceptible to opportunistic infections (Ammann, 1991). As mentioned above, chronic malnutrition following World War II resulted in PCP in Eastern European children (Walzer, 1990). Transplant recipients treated with immunosuppressive drugs such as cyclosporin and glucocorticoids often suffer recurrent diseases due to pathogens such as varicella zoster virus and cytomegalovirus that also cause disease in HIV-infected individuals (Chandra, 1983; Ammann, 1991).

However, the specific immunologic profile that typifies AIDS--a progressive reduction of CD4+ T cells resulting in persistent CD4+ T lymphocytopenia and profound deficits in cellular immunity--is extraordinarily rare in the absence of HIV infection or other known causes of immunosuppression. This was recently demonstrated in several surveys that sought to determine the frequency of idiopathic CD4+ T-cell lymphocytopenia (ICL), which is characterized by CD4+ T cell counts lower than 300 cells per cubic millimeter (mm3) of blood in the absence of HIV antibodies or conditions or therapies associated with depressed levels of CD4+ T cells (reviewed in Fauci, 1993b; Laurence, 1993).

In a CDC survey, only 47 (.02 percent) of 230,179 individuals diagnosed with AIDS were both HIV-seronegative and had persistently low CD4+ T cell counts (3) IN THE ABSENCE OF CONDITIONS OR THERAPIES ASSOCIATED WITH IMMUNOSUPPRESSION (SMITH ET AL., 1993).

In the MACS, 22,643 CD4+ T cell determinations in 2,713 HIV-seronegative homosexual men revealed only one individual with a CD4+ T cell count persistently lower than 300 cells/mm3, and this individual was receiving immunosuppressive therapy (Vermund et al., 1993a). A similar review of another cohort of homosexual and bisexual men found no case of persistently lowered CD4+ T cell counts among 756 HIV-seronegative men who had no other cause of immunosuppression (Smith et al., 1993). Analogous results were reported from the San Francisco Men's Health Study, a population-based cohort recruited in 1984. Among 206 HIV-seronegative heterosexual and 526 HIV-seronegative homosexual or bisexual men, only one had consistently low CD4+ T cell counts (Sheppard et al., 1993). This individual also had low CD8+ T cell counts, suggesting that he had general lymphopenia rather than a selective loss of CD4+ T cells. No AIDS-defining clinical condition was observed among these HIV-seronegative men.

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Studies of blood donors, recipients of blood and blood products, and household and sexual contacts of transfusion recipients also suggest that persistently low CD4+ T cell counts are extremely rare in the absence of HIV infection (Aledort et al., 1993; Busch et al., 1994). Longitudinal studies of injection-drug users have demonstrated that unexplained CD4+ T lymphocytopenia is almost never seen among HIV-seronegative individuals in this population, despite a high risk of exposure to hepatitis B, cytomegalovirus and other blood-borne pathogens (Des Jarlais et al., 1993; Weiss et al., 1992).





  
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