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AIDS Immunopathogenesis Unit, Department of Biology and Technology, and
Laboratory of Clinical Immunology, Division of Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy;
IRIS Research Center, Chiron SpA, Siena, Italy; and
Picower Institute for Medical Research, Manhasset, NY 11030
We have recently shown that the binding subunit of pertussis toxin
(PTX-B) inhibits the entry and replication of macrophage-tropic (R5)
HIV-1 strains in activated primary T lymphocytes. Furthermore, PTX-B
suppressed the replication of T cell-tropic (X4) viruses at a postentry
level in the same cells. In this study we demonstrate that PTX-B
profoundly impairs entry and replication of the HIV-1ADA
(R5), as well as of HIV pseudotyped with either murine leukemia virus
or vesicular stomatitis virus envelopes, in primary monocyte-derived
macrophages. In addition, PTX-B strongly inhibited X4 HIV-1 replication
in U937 promonocytic cells and virus expression in the U937-derived
chronically infected U1 cell line stimulated with cytokines such as
TNF-
and IL-6. Of interest, TNF--mediated activation of the
cellular transcription factor NF-
B was unaffected by PTX-B.
Therefore, PTX-B may represent a novel and potent inhibitor of HIV-1
replication to be tested for efficacy in infected individuals. In
support of this proposition, a genetically modified mutant of PTX
(PT-9K/129G), which is safely administered for prevention of
Bordetella pertussis infection, showed an
in vitro anti-HIV profile superimposable to that of
PTX-B.
This article has been cited by other articles:
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