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*
Department of Medical Microbiology, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Ireland;
Rockefeller University, New York, NY 10021; and
North Shore Hospital System, Manhassett, NY 11030
To investigate the immunological features of human T lymphotropic
virus type II (HTLV-II) infection and specific mechanisms whereby
HTLV-II might influence the progression of HIV-1 disease in coinfected
individuals, we have analyzed the production of the C-C chemokines
RANTES and macrophage inflammatory proteins 1
and 1ß (MIP-1 and
MIP-1ß) by PBMCs from HTLV-II-infected and HTLV-II/HIV-1-coinfected
individuals. We observed spontaneous production of significant levels
of MIP-1 and -1ß and, to a lesser extent, RANTES, from individuals
infected with HTLV-II alone or with concomitant HIV-1 infection.
Spontaneous C-C chemokine production was not observed in PBMCs from
uninfected or HIV-1-infected individuals. Although HTLV-II is known to
preferentially infect CD8+ lymphocytes in vivo, we observed
that whereas RANTES was produced exclusively by the
CD8+-enriched fraction, MIP-1 and -1ß were produced by
both the CD8+-enriched and CD8+-depleted
fractions of HTLV-II-infected PBMCs. RT-PCR demonstrated active
expression of the HTLV-II regulatory protein Tax in the infected
CD8+ T lymphocyte population, and it was further shown that
Tax transactivates the promoters of MIP-1ß and RANTES. Therefore, it
appears that HTLV-II stimulates the production of C-C chemokines both
directly at a transcriptional level via the viral transactivator Tax
and also indirectly. Although the HTLV-II-infected individuals in this
study are all virtually asymptomatic, they certainly display an
abnormal immune phenotype. Moreover, our findings suggest that HTLV-II,
via chemokine production, would be expected to alter the progression of
HIV-1 infection in coinfected individuals.
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