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lüll Mechanisms underlying activity of antiretroviral drugs in HIV-1-infected macrophages: new therapeutic strategies Aquaro S; Svicher V; Schols D; Pollicita M; Antinori A; Balzarini J; Perno CFJ Leukoc Biol 2006[Nov]; 80 (5): 1103-10Monocyte-derived macrophages (M/M) are considered the second cellular target of HIV-1 and a crucial virus reservoir. M/M are widely distributed in all tissues and organs, including the CNS, where they represent the most common HIV-infected cells. Differently from activated CD4+ T lymphocytes, M/M are resistant to the cytopathic effect of HIV and survive HIV infection for a long time. Moreover, HIV-1 replication in M/M is a key pathogenetic event during the course of HIV-1 infection. Overall findings strongly support the clinical relevance of anti-HIV drugs in M/M. Nucleoside RT inhibitors (NRTIs) are more active against HIV in M/M than in CD4+ T lymphocytes. Their activity is further boosted by the presence of an additional monophosphate group (i.e., a phosphonate group, as in the case of Tenofovir), thus overcoming the bottleneck of the low phosphorylation ability of M/M. In contrast, the antiviral activity of non-NRTIs (not affecting the DNA chain elongation) in M/M is similar to that in CD4+ T lymphocytes. Protease inhibitors are the only clinically approved drugs acting at a late stage of the HIV lifecycle. They are able to interfere with HIV replication in HIV-1 chronically infected M/M, even if at concentrations greater than those observed in HIV-1 chronically infected CD4+ T lymphocytes. Finally, several new drugs have been shown to interfere efficiently with HIV replication in M/M, including entry inhibitors. A better understanding of the activity of the anti-HIV drugs in M/M may represent a key element for the design of effective anti-HIV chemotherapy.|Anti-HIV Agents/*pharmacology/therapeutic use[MESH]|CD4-Positive T-Lymphocytes/drug effects/virology[MESH]|HIV Infections/drug therapy/*immunology[MESH]|HIV-1/*drug effects[MESH]|Humans[MESH]|Macrophages/*drug effects/virology[MESH]|Microbial Sensitivity Tests[MESH]|Structure-Activity Relationship[MESH]|Virus Replication/drug effects[MESH] |