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* Department of Immunology and Infectious Disease, San Raffaele Scientific Institute, Milan, Italy;
Department of Clinical Medicine, Nephrology, and Health Sciences, University of Parma, Parma, Italy; and
Department of Mother and Child, Biology and Genetic Section, University of Verona, Verona, Italy
Human T cell leukemia virus (HTLV) type-2 is a human retrovirus
whose infection has not been tightly linked to human diseases. However,
the fairly high prevalence of this infection among HIV-1-positive
individuals indicates the importance of better understanding the
potential interference of HTLV-2 infection on HIV-1 infection and AIDS.
We previously demonstrated that one signature of PBMC freshly derived
from HIV-1-infected individuals is the constitutive activation of a
C-terminal truncated STAT5 (STAT5
). Therefore, we analyzed the
potential activation of STATs in HTLV-2 monoinfected and HTLV-2/HIV-1
dually infected individuals. We observed that PBMC of HTLV-2-infected
individuals do not show STAT activation unless they are cultivated ex
vivo, in the absence of any mitogenic stimuli, for at least 8 h.
The emergence of STAT activation, namely of STAT1, in culture was
mostly related to the secretion of IFN-
. Of note, this phenomenon is
not only a characteristic feature of HTLV-2-infected individuals but
also occurred with PBMC of HIV-1+ individuals.
Surprisingly, HTLV-2/HIV-1 coinfection resulted in low/absent STAT
activation in vivo that paralleled a diminished secretion of IFN-
after ex vivo cultivation. Our findings indicate that both HTLV-2 and
HIV-1 infection prime T lymphocytes for STAT1 activation, but they also
highlight an interference exerted by HTLV-2 on HIV-1-induced STAT1
activation. Although the nature of such a phenomenon is unclear at the
present, these findings support the hypothesis that HTLV-2 may
interfere with HIV-1 infection at multiple
levels.
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