The Relationship between the Human Immunodeficiency Virus and the Acquired Immunodeficiency Syndrome (Draft)

DRAFT

The emergence of HIV variants that are more cytopathic and replicate in a wider range
of susceptible cells in vitro has also been shown to correlate with disease progression in HIVinfected individuals (Fenyo et al., 1988; Tersmette et al., 1988, 1989a,b; Richman and
Bozzette, 1994; Connor et al., 1993, 1994a,b;). Similar results have been seen in vivo with
macaques infected with molecularly cloned SIV (Kodama et al., 1993). It has also been
reported that HIV isolates from patients who progress to AIDS have a higher rate of replication
compared with HIV isolates from individuals who remain asymptomatic (Fenyo, et al. 1988;
Tersmette et al., 1989a). For example, in series of sequential isolates taken from individuals
throughout the course of HIV infection, rapidly replicating variants of HIV emerged during the
asymptomatic stage of disease prior to disease progression (Tersmette et al., 1989b; Connor
and Ho, 1994b).
Immunologic Profile in 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 Eastem 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). However, the specific immunologic
profile that typifies AIDS -- a progressive reduction of CD4+ T cells resulting in persistent
CD4+ lymphocytopenia and profound deficits in cellular imunity -- 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

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