Biology Reference
In-Depth Information
T A B L E 3.1. A Brief Summary of the Main Changes Observed When
Immunophenotyping Is Performed in Cells of HIV-Infected Patients
CD45RO CD45RA CD95 CD25 CD38 HLADR CD57 CD69 CD7 SLAM
CD4
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CD8
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(CD95), CD25, CD38, HLA-DR, CD57, and CD69 and decrease in the
subpopulations expressing CD45RA, CD7, and signaling lymphocytic
activation molecule (SLAM)
± CD8
T cells increase in the subpopulations expressing CD38,
CD45RO, CD57, and CD69 and decrease in the subpopulations ex-
pressing CD45RA and CD28
± NK cells increase in the subpopulations expressing CD56 and decrease in
the CD16/CD56 subpopulations
HIV infection ultimately results in the appearance of the acquired immuno-
de®ciency syndrome (AIDS); the diagnosis of AIDS was, until the introduction
of highly active antiretroviral therapy ( HAART ), shortly thereafter followed
by death.
In this chapter we will brie¯y summarize the defects in T-helper functions
and phenotype induced by HIV infection as well as the e¨ects of HAART on
immune reconstitution.
FUNCTIONAL IMMUNE DYSREGULATION IN HIV INFECTION
Primary HIV infection can be asymptomatic or can be associated with a ¯u-like
syndrome characterized by fever, malaise, and weakness ( Kahn and Walker,
1998). The early phase of HIV infection is also always correlated with the
presence of extremely elevated titers of HIV in the plasma (Ho et al., 1994).
A potent HIV-speci®c immune response is rapidly induced within a few days
after primary infection. In this phase, both humoral immunity ( HI) and cell-
mediated immunity (CMI ) are promptly stimulated. It was nevertheless con-
vincingly demonstrated that a signi®cant reduction in HIV plasma viremia de-
pends on the generation of an HIV-speci®c cell-mediated immune response,
independently of the magnitude of the humoral immune response (Borrow et
al., 1994; Poignard et al., 1999). This concept is mostly based on the observa-
tion that the detection of HIV-speci®c cytotoxic T lymphocyte (CTL) precedes
reductions in viral load, whereas the generation of neutralizing antibodies is
delayed and is observed after the changes in HIV viremia has taken place
( Borrow et al., 1994). The idea that the modulation of HIV replication is asso-
ciated with an intact and powerful HIV-speci®c CMI (Clerici and Shearer,
