Centre de Recherche en Infectiologie, Centre Hospitalier Universitaire de Québec, Pavillon CHUL, and Département de Biologie Médicale, Faculté de Médecine, Université Laval, Ste-Foy, Québec, Canada
Correspondence: Michel J. Tremblay, Centre de Recherche en Infectiologie, RC709, Centre Hospitalier Universitaire de Québec, Pavillon CHUL, 2705 boul. Laurier, Ste-Foy, Québec, Canada G1V 4G2. E-mail: Michel.J.Tremblay{at}crchul.ulaval.ca
Throughout the years, most researchers have used continuous cell lines
as in vitro models to evaluate the immunopathogenesis of
human immunodeficiency virus type-1 (HIV-1) infection. Unfortunately,
the most commonly used monocytoid malignant cells have not been shown
to adequately mimic primary human monocyte-derived macrophages, at
least with respect to HIV-1 infection. The Mono Mac 1 cell line has
been defined as a model system for studying biochemical, immunological,
and genetic functions of human cells of the monocyte/macrophage
lineage. In this study, we have investigated whether Mono Mac 1
represents an in vitro culture system for HIV-1 infection.
Flow cytometric analyses revealed that Mono Mac 1 are positive for the
HIV-1 primary receptor (CD4), as well as for the coreceptors (CXCR4,
CCR5, and CCR3). Infectivity experiments conducted with recombinant
luciferase-encoding and fully infectious viruses demonstrated that Mono
Mac 1 can support a highly productive infection with both macrophage-
and dual-tropic isolates of HIV-1. Furthermore, differentiation of such
cells led to a marked increase in virus production. Data from
semiquantitative polymerase chain reaction analysis and mobility shift
assays indicated that enhanced virus production in differentiated Mono
Mac 1 cells was most likely related to an increase in nuclear
translocation of NF-
B. Mono Mac 1 can thus be considered as a human
monocytoid cell line representing a proper in vitro system
for studying the complex interactions between HIV-1 and cells of the
monocyte/macrophage lineage.
Key Words: monocytes/macrophages AIDS/HIV cellular differentiation cell surface molecules transcription factors
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