Clinical AIDS

The stage of clinical AIDS that is reached years after initial infection is marked by the appearance of one or more of the typical opportunistic infections or neoplasms diagnostic of AIDS by definitional criteria. The progression to clinical AIDS is also marked by the appearance of syncytia-forming (SI) variants of HIV in about half of HIV infected patients. These SI viral variants, derived from non-syncytia-forming (NSI) variants, have greater CD4 cell tropism and are associated with more rapid CD4+ cell decline. The SI variants typically arise in association with a peripheral blood CD4 lymphocyte count between 400 and 500/microliter, prior to the onset of clinical AIDS. However, appearance of the SI phenotype of HIV is a marker for progression to AIDS that is independent of CD4 cell counts.
Other laboratory findings which indicate progression to AIDS include HIV p24 antigen positivity, increased serum beta2-microglobulin, elevated serum IgA, or increased neopterin levels in serum, cerebrospinal fluid, or urine. The p24 antigen is a highly specific predictor of progression, but only about 60% of HIV-infected persons develop p24 antigenemia prior to onset of clinical AIDS. Beta2-microglobulin is increased with lymphocyte activation or destruction associated with HIV disease progression. Neopterin, as measured in serum or urine, is also a measure of immune system activation and can predict HIV disease progression. The information provided by these tests is similar, so no advantage accrues from performing all of them simultaneously.
For perinatally acquired HIV infection, the time to development of clinical AIDS may be shorter than in adults. Signs associated with HIV infection appear in over 80% of seropositive infants by the age of 5 months. Infants in whom such signs appear at 3 months tend to have decreased survival. About half of children with perinatally acquired HIV infection are alive at 9 years.