title: Plastic restriction of HIV-1 replication in human macrophages derived from M1/M2 polarized monocytes.
abstract: M1/M2 cytokine-dependent polarization of primary human MDMs has been shown to contain CCR5-dependent (R5) HIV-1 replication. In this study, a similar effect was achieved when monocytes were first polarized toward M1 or M2 and were infected 7 d after their differentiation into MDMs, regardless of whether the cytokines were removed 18 h after cell stimulation or were left in culture. Unlike polarized MDMs, no significant down-regulation of CD4 from the cell surface was observed in MDMs derived from M1/M2-polarized monocytes. A second stimulation of MDMs differentiated from M1/M2 monocytes with the opposite polarizing cytokines converted the virus replication profile according to the new stimuli. The expression of M1 and M2 markers (i.e., APOBEC3A and DC-SIGN, respectively) was induced by MDM stimulation with the opposite cytokines, although it also persisted in cells according to their first stimulatory condition. Thus, stimulation of monocytes with M1- and M2-inducing cytokines leads to a restriction of HIV-1 replication when these cells are infected several days later as differentiated MDMs. These observations imply that activation of circulating monocytes significantly influences their capacity to either support or restrict HIV-1 replication, once extravasated, and eventually to become infected as tissue macrophages.
authors.affiliation: AIDS Immunopathogenesis Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milano, Italy.
authors.forename: Francesca
authors.initials: F
authors.lastname: Graziano
authors.affiliation: Viral Pathogens and Biosafety Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milano, Italy.
authors.forename: Elisa
authors.initials: E
authors.lastname: Vicenzi
authors.affiliation: AIDS Immunopathogenesis Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milano, Italy; poli.guido@hsr.it.|School of Medicine, Vita-Salute San Raffaele University, Milano, Italy; and.|Institute of Human Virology, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
authors.forename: Guido
authors.initials: G
authors.lastname: Poli
mesh_terms: D000943:Antigens, Differentiation / Q000096:biosynthesis; D015815:Cell Adhesion Molecules / Q000096:biosynthesis / Q000235:genetics; D002454:Cell Differentiation; D003564:Cytidine Deaminase / Q000096:biosynthesis / Q000235:genetics; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology; D015847:Interleukin-4 / Q000494:pharmacology; D037181:Lectins, C-Type / Q000096:biosynthesis / Q000235:genetics; D008264:Macrophages / Q000145:classification / Q000821:virology*; D009000:Monocytes / Q000166:cytology*; D011506:Proteins / Q000235:genetics; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000235:genetics; D011994:Recombinant Proteins / Q000494:pharmacology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D014779:Virus Replication; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin
chemical_list: D000943:Antigens, Differentiation; D015815:Cell Adhesion Molecules; D003564:Cytidine Deaminase; D007371:Interferon-gamma; D015847:Interleukin-4; D037181:Lectins, C-Type; D011506:Proteins; D011956:Receptors, Cell Surface; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin; C121399:APOBEC3A protein, human
keywords: APOBEC3A/3G; CD4; DC-SIGN; viral entry; viral latency