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Due to a higher possibility of virologic failure, these regimens are generally not allowed in this clinical setting. In antiretroviral-experienced patients, dual regimens are examined in studies with a small sample size, centered on clinical practice, and should be ritonavir-boosted protease inhibitor-based. These combinations have a good virological efficacy; combinations with the integrase inhibitor raltegravir have small sample size and demonstrated efficacy only with etravirine. Virological aspects involving dual therapy should always consider genetic barriers, particularly in simplification strategies, and ritonavir-boosted protease inhibitors are mandatory. As far as immunological aspects are concerned, nucleoside reverse transcriptase inhibitor-sparing regimens have some encouraging data, probably due to the bone marrow toxicity of this class. Combinations with maraviroc were effective in reducing inflammation, but data about immunological recovery are conflicting. The choice of regimen should focus on specific class toxicity since dual regimens are studied in particular for improving safety and tolerability. This review will analyze different dual regimens in the clinical setting, with a peculiar focus on ameliorating toxicities and improving quality of life.";s:9:"metadata5";s:40:"State of the Art of Dual Therapy in 2015";s:9:"metadata6";s:121:"Nozza, S; Svicher, V; Saracino, A; d'Ettorre, G; De Luca, A; Maggiolo, F; Bonora, S; di Biagio, A; Rusconi, S; Mussini, C";s:9:"metadata7";N;s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:50;a:14:{s:9:"citazione";s:308:"Pollicita, M., Alteri, C., Bellocchi, M.C., Armenia, D., Carioti, L., Salpini, R., et al. (2015). A recent epidemiological cluster of acute hepatitis B genotype F1b infection in a restricted geographical area of Italy. 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Reliable timescale inference of HBV genotype A origin and phylodynamics. INFECTION GENETICS AND EVOLUTION, 32, 361-369 [10.1016/j.meegid.2015.03.009].";s:4:"data";s:4:"2015";s:2:"id";s:20:"PUBBLICAZIONE_384144";s:6:"handle";s:11:"2108/242523";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore MED/07";s:9:"metadata4";N;s:9:"metadata5";s:71:"Reliable timescale inference of HBV genotype A origin and phylodynamics";s:9:"metadata6";s:184:"Zehender, G; Svicher, V; Gabanelli, E; Ebranati, E; Veo, C; Lo Presti, A; Cella, E; Giovanetti, M; Bussini, L; Salpini, R; Alteri, C; Lai, A; Tanzi, E; Perno, CF; Galli, M; Ciccozzi, M";s:9:"metadata7";s:28:"10.1016/j.meegid.2015.03.009";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:52;a:14:{s:9:"citazione";s:304:"Mirabelli, C., Surdo, M., Van Hemert, F., Lian, Z., Salpini, R., Cento, V., et al. (2014). Specific mutations in the C-terminus domain of HBV surface antigen significantly correlate with low level of serum HBV-DNA in patients with chronic HBV infection. 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(2014). Detection of high levels of Survivin-immunoglobulin M immune complex in sera from hepatitis C virus infected patients with cirrhosis. 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The multifactorial pathways towards resistance to the cytosine analogues emtricitabine and lamivudine: Evidences from literature. JOURNAL OF INFECTION [10.1016/j.jinf.2014.05.001].";s:4:"data";s:10:"2014-05-15";s:2:"id";s:20:"PUBBLICAZIONE_185038";s:6:"handle";s:10:"2108/89696";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:54:"Settore MED/07 - Microbiologia e Microbiologia Clinica";s:9:"metadata4";N;s:9:"metadata5";s:128:"The multifactorial pathways towards resistance to the cytosine analogues emtricitabine and lamivudine: Evidences from literature";s:9:"metadata6";s:94:"Svicher, V; Alteri, C; Santoro, M; Ceccherini-Silberstein, F; Marcelin, A; Calvez, V; Perno, C";s:9:"metadata7";s:26:"10.1016/j.jinf.2014.05.001";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:58;a:14:{s:9:"citazione";s:275:"Svicher, V., Alteri, C., Montano, M., Nori, A., D'Arrigo, R., Andreoni, M., et al. (2014). Genotypic testing on HIV-1 DNA as a tool to assess HIV-1 co-receptor usage in clinical practice: results from the DIVA study group. 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(2014). Highlights on HIV eradication in 2013. AIDS, 28(1), 1-7.";s:4:"data";s:10:"2014-01-02";s:2:"id";s:20:"PUBBLICAZIONE_185027";s:6:"handle";s:10:"2108/89709";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:54:"Settore MED/07 - Microbiologia e Microbiologia Clinica";s:9:"metadata4";N;s:9:"metadata5";s:37:"Highlights on HIV eradication in 2013";s:9:"metadata6";s:70:"Monforte, A; Svicher, V; Nozza, S; Lazzarin, A; Marchetti, G; Perno, C";s:9:"metadata7";s:35:"10.1097/01.aids.0000433241.78739.79";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:60;a:14:{s:9:"citazione";s:264:"Surdo, M., Balestra, E., Saccomandi, P., Di Santo, F., Montano, M., Di Carlo, D., et al. (2013). Inhibition of dual/mixed tropic HIV-1 isolates by CCR5-inhibitors in primary lymphocytes and macrophages. 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Structural modifications induced by specific HIV-1 protease-compensatory mutations have an impact on the virological response to a first-line lopinavir/ritonavir-containing regimen. 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(2013). Detecting and understanding genetic and structural features in HIV-1 B subtype V3 underlying HIV-1 co-receptor usage. BIOINFORMATICS, 29(4), 451-460 [10.1093/bioinformatics/btt002].";s:4:"data";s:10:"2013-02-15";s:2:"id";s:20:"PUBBLICAZIONE_158915";s:6:"handle";s:10:"2108/75768";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:54:"Settore MED/07 - Microbiologia e Microbiologia Clinica";s:9:"metadata4";N;s:9:"metadata5";s:116:"Detecting and understanding genetic and structural features in HIV-1 B subtype V3 underlying HIV-1 co-receptor usage";s:9:"metadata6";s:122:"Chen, M; Svicher, V; Artese, A; Costa, G; Alteri, C; Ortuso, F; Parrotta, L; Liu, Y; Liu, C; Perno, C; Alcaro, S; Zhang, J";s:9:"metadata7";s:29:"10.1093/bioinformatics/btt002";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:65;a:14:{s:9:"citazione";s:230:"Santoro, M., Armenia, D., Alteri, C., Flandre, P., Calcagno, A., Santoro, M., et al. (2013). Impact of pre-therapy viral load on virological response to modern first-line HAART. 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The genotypic false positive rate determined by V3 population sequencing can predict the burden of HIV-1 CXCR4-using species detected by pyrosequencing. 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Overlapping structure of HBV genome and immune selection pressure are critical forces modulating HBV evolution. 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The lowest X4 Geno2Pheno false-positive rate is associated with greater CD4 depletion in HIV-1 infected patients. 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Novel HBsAg markers tightly correlate with occult HBV infection and strongly affect HBsAg detection. 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Novel reverse transcriptase mutations specifically associated with selected anti-Hbv treatment can induce alterations and stop-codons in Hbv S antigen. 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Lamivudine-resistance mutations can be selected even at very low levels of hepatitis B viraemia. 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