A. Kinter et As. Fauci, INTERLEUKIN-2 AND HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION - PATHOGENICMECHANISMS AND POTENTIAL FOR IMMUNOLOGICAL ENHANCEMENT, Immunologic research, 15(1), 1996, pp. 1-15
A hallmark of human immunodeficiency virus (HIV) infection is the prog
ressive loss of CD4+ T lymphocytes; however, qualitative defects in im
mune responses occur prior to the precipitous drop CD4+ T cell numbers
. One of the first immunologic defects to be described in HIV-infected
individuals is a deficiency in interleukin (IL)-2 production. The add
ition of IL-2 in vitro to cultures of mononuclear cells from HIV-infec
ted individuals partially or completely restored certain defective cel
lular immune responses, However, production of or addition of IL-2 has
also been associated with increased viral replication in infected T c
ells. These observations underscore the pernicious correlation between
immune activation and HIV replication. However, recent in vitro and i
n vivo studies have provided promising preliminary results suggesting
that, at least at certain stages of disease, the benefits of IL-2-medi
ated immune enhancement may outweigh or override the inductive effects
of this cytokine on HIV production.