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Blood, Vol. 95 No. 9 (May 1), 2000:
pp. 2760-2769
HTLV-II down-regulates HIV-1 replication in IL-2-stimulated
primary PBMC of coinfected individuals through expression of
MIP-1
Claudio Casoli,
Elisa Vicenzi,
Andrea Cimarelli,
Giacomo Magnani,
Paolo Ciancianaini,
Ercole Cattaneo,
PierPaolo Dall'Aglio,
Guido Poli, and
Umberto Bertazzoni
From the Istituto di Patologia Medica, Università di Parma,
Parma; Unità di Immunopatogenesi dell'AIDS, Istituto Scientifico
San Raffaele, Milano; Istituto di Genetica Biochimica ed
Evoluzionistica del CNR, Pavia; Divisione di Malattie Infettive,
Ospedale di Parma, Parma; Laboratorio Retrovirus, IRCCS Policlinico S. Matteo, Pavia; and Sezione di Biologia e Genetica DMIBG,
Università di Verona, Italy.
The influence of human T-cell leukemia/lymphoma virus type II
(HTLV-II) in individuals also infected with HIV-1 is poorly understood.
To evaluate the reciprocal influence of HTLV-II and HIV-1 infection,
primary peripheral blood mononuclear cell (PBMC) cultures from
coinfected individuals were established in the presence of interleukin
2 (IL-2). In these cultures, the kinetics of HTLV-II replication
always preceded those of HIV-1. Noteworthy, the kinetics of HIV-1
production were inversely correlated to the HTLV-II proviral load in
vivo and its replication ex vivo. These observations
suggested a potential interaction between the 2 retroviruses. In
this regard, the levels of IL-2, IL-6, and tumor necrosis factor-
(TNF-) were measured in the same coinfected PBMC cultures.
Endogenous IL-2 was not produced, whereas IL-6 and TNF- were
secreted at levels compatible with their known ability to up-regulate
HIV-1 expression. The HIV-suppressive CC-chemokines RANTES, macrophage inflammatory protein-1 (MIP-1), and MIP-1 were also determined in IL-2-stimulated PBMC cultures. Of interest, their kinetics and
concentrations were inversely related to those of HIV-1 replication. Experiments were performed in which CD8+ T cells or PBMCs
from HTLV-II monoinfected individuals were cocultivated with
CD4+ T cells from HIV-1 monoinfected individuals
separated by a semipermeable membrane in the presence or absence of
antichemokine neutralizing antibodies. The results indicate that
HTLV-II can interfere with the replicative potential of HIV-1 by
up-regulating viral suppressive CC-chemokines and, in particular,
MIP-1. This study is the first report indicating that HTLV-II can
influence HIV replication, at least in vitro, via up-regulation of
HIV-suppressive chemokines.
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