The monocyte/macrophage system, which is characterized by a high degree of heterogeneity, is a target of the human immunodeficiency virus (HIV) in vitro as well as in vivo. Both bone-marrow-derived precursor elements and circulating monocytes are infectable in vitro and have also been found infected in seropositive individuals. However, terminally differentiated macrophages are the most commonly infected cells found in vivo in addition to the CD4+ T lymphocytes. Several immunoregulatory cytokines have been shown to either up-regulate or suppress virus replication/expression in vitro in cells belonging to the monocyte/macrophage lineage by affecting both transcriptional as well as posttranscriptional events. The observation that elevated levels of several of these cytokines are present in HIV-infected individuals suggests that they may play an important role as regulators of virus expression in vivo.
THE ROLE OF MONOCYTE MACROPHAGES AND CYTOKINES IN THE PATHOGENESIS OF HIV-INFECTION
POLI , GUIDO;
1992-01-01
Abstract
The monocyte/macrophage system, which is characterized by a high degree of heterogeneity, is a target of the human immunodeficiency virus (HIV) in vitro as well as in vivo. Both bone-marrow-derived precursor elements and circulating monocytes are infectable in vitro and have also been found infected in seropositive individuals. However, terminally differentiated macrophages are the most commonly infected cells found in vivo in addition to the CD4+ T lymphocytes. Several immunoregulatory cytokines have been shown to either up-regulate or suppress virus replication/expression in vitro in cells belonging to the monocyte/macrophage lineage by affecting both transcriptional as well as posttranscriptional events. The observation that elevated levels of several of these cytokines are present in HIV-infected individuals suggests that they may play an important role as regulators of virus expression in vivo.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.