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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 (<300/MM3) 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.
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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