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1. Antiretroviral genotypic resistance in plasma RNA and whole blood DNA in HIV-1 infected patients failing HAART

Author

Saracino, A, Gianotti, N, Marangi, M, Cibelli, Dc, Galli, A, Punzi, G, Monno, L, Lazzarin, A, Angarano, G, Dini, M, Del Gobbo, R, Montroni, M, Butini, L, Scalise, G, Ancarani, F, Di Cesare, S, Giacometti, A, Biglino, A, Degioanni, M, Paoloni, M, Mariani, R, Calella, G, Pastore, G, Ladisa, N, Mennea, G, Gritti, Fm, Fasullo, G, Chiodo, F, Borderi, M, Carosi, Giampiero, Castelli, Francesco, Torti, Carlo, Uccelli, C, Rizzardini, G, Visoná, R, Salvo, A, Averna, A, Russo, R, Celesia, Bm, Cosentino, S, Rinaldi, E, Pusterla, L, Carnevale, G, Mondello, P, Petrini, C, Ghinelli, F, Sighinolfi, L, Mazzotta, F, Lo Caputo, S, Pierotti, P, Leoncini, F, Sterrantino, Gk, Corsi, P, Pompei, Ag, Di Toro MT, Purificato, F, Indiveri, F, Setti, M, Murdaca, G, Iannessi, A, Cellini, A, Mariani, A, Scasso, A, De Gennaro, M, Chiodera, A, Castelli, P, Maltempo, K, Mongolo, G, Caggese, L, Schlacht, I, Cargnel, A, Atzori, C, Micheli, V, Moroni, M, Bini, T, Marcatto, I, Chiesa, E, Vigevani, G, Argenteri, B, Capetti, A, Esposito, R, Guaraldi, G, Seghetto, B, Chirianni, A, Gargiulo, M, Abrescia, N, D'Abbraccio, M, Busto, T, Marchitelli, C, Santirocchi, M, Abbadessa, V, Mancuso, S, Meneghetti, F, Pranzetti, M, Ferrari, C, Pizzaferri, P, Stagni, G, Di Candilo, F, Petrelli, E, Balducci, M, Menichetti, F, Polidori, M, Tascini, C, Di Carlo, A, Palamara, G, Antinori, A, Liuzzi, G, Aiuti, F, Mezzaroma, I, Pinter, E, Barbone, B, Vullo, V, Massetti, P, Dell'Isola, S, Mura, Ms, Mannazzu, M, Delias, R, Di Giammartino, D, Tarquini, P, Marranconi, F, Ferretto, R, Caramello, P, Orofino, Gc, Cimino, T, Bramato, C, Di Perri, G, Sinicco, A, Zeme, D, Bonora, S, Trentini, L, Soranzo, Ml, Macor, A, Salassa, B, Branz, F, Delle Foglie, P, Vaglia, A, Rossi, Mc, Ciccone, L, Panzolli, L, Grossi, P, Giola, M, Raise, E, Narne, E, Poggio, A, Demin, F, Mondino, V, Serpelloni, G, Malena, M, Bosco, O., Saracino, A, Gianotti, N, Marangi, M, Cibelli, D, Galli, A, Punzi, G, Monno, L, Lazzarin, A, Angarano, G, and Mancuso, S

Subjects
Anti-HIV Agents, DNA Mutational Analysis, Molecular Sequence Data, Proviral DNA, HIV Infections, HAART failure, medicine.disease_cause, DNA Mutational Analysi, chemistry.chemical_compound, HIV Protease, Proviruses, Antiretroviral Therapy, Highly Active, Virology, Drug Resistance, Viral, medicine, Humans, Multicenter Studies as Topic, HIV Infection, Treatment Failure, Genotyping, Randomized Controlled Trials as Topic, COLD-PCR, Mutation, Plasma RNA, biology, Proviruse, Sequence Analysis, RNA, Anti-HIV Agent, RNA, Sequence Analysis, DNA, biology.organism_classification, HIV Reverse Transcriptase, Reverse transcriptase, Antiretroviral genotypic resistance, Infectious Diseases, chemistry, DNA, Viral, Lentivirus, Immunology, HIV-1, RNA, Viral, DNA, antiretroviral genotypic resistance, haart failure, hiv-1, plasma rna, proviral dna, Human
Abstract

The extent to which HIV-1 proviral DNA mutations cause clinically relevant antiretroviral resistance is still controversial. Paired plasma HIV-1 RNA and whole blood DNA were compared in patients failing HAART to investigate if the additional knowledge of archived mutations could improve the selection of potentially active drugs. Seventy-three HIV-1-infected patients with first/second HAART failure were studied before starting a new regimen based on RNA genotyping. Follow-up data after a 12-week therapy were available. DNA genotyping was retrospectively performed on stored whole blood samples and mutational profiles were compared to those from RNA. The mean number of IAS pol mutations was significantly higher in RNA (4.45 ± 2.76) than in DNA (2.88 ± 2.47) (P < 0.001). DNA genotyping provided a 6% increase in detection of resistance-associated mutations. Among 64/73 patients showing discordant DNA/RNA profiles, 54 (84%) also differed for predicted active drugs. 16/73 (22%) patients had ≥1 mutation revealed by DNA genotyping alone, probably affecting therapy success in 2/16. However, neither RNA/DNA discordance nor detection of isolated DNA mutations were statistically associated with outcome. In conclusion, plasma RNA remains the elective choice for HIV genotyping in patients with therapy failure, even if the detection of proviral resistance-associated mutations, not simultaneously found in RNA, is a frequent event. Therefore, in some cases DNA plus RNA genotyping might assist in choosing more accurately subsequent antiretroviral regimens. © 2008 Wiley-Liss, Inc.

Published
2008
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2. Replication capacity in relation to immunologic and virologic outcomes in HIV-1-infected treatment-naive subjects

Author

Skowron, G, Spritzler, Jg, Weidler, J, Robbins, Gk, Johnson, Va, Chan, Es, Asmuth, Dm, Gandhi, Rt, Lie, Y, Bates, M, Pollard, Rb, NIH/NIAID ACTG 384 Protocol Team, Monogram, Biosciences, Vella, S, Chiesi, C, Arcieri, R, Pirillo, Mf, Galluzzo, Cm, Pia Germinario EA, Amici, R, Marzi, M, Nobile, A, Di Nallo, R, Polizzi, C, Coronado, O, Fasulo, G, Carosi, Giampiero, Castelli, Francesco, Di Pietro, M, Vichi Ospedale, F, Sterrantino, G, Ambu, S, Cargnel, A, Meraviglia, P, Niero, F, Capetti, A, d'Arminio Monforte, A, Sollima, S, Balotta, C, Delia, S, Ciardi, M, Soranzo, Ml, Macor, A, D'Ettorre, G, Forcina, G, Bassetti, D, Di Biagio, A, Minoli, L, Maserati, R, Ghinelli, F, Sighinolfi, L, Riva, A, Scalise, G, Santoro, D, Rinaldi, E, Chiodo, F, Borderi, M, Guaraldi, G, Esposito, R, Ferrari, C, Pasetti, G, Abrescia, N, Busto, A, Chirianni, A, Gargiulo, M, Izzo, Cm, Sbreglia, C, Alberici, F, Sacchini, D, Magnani, G, and Zoboli, G.

Subjects
Adult, Male, medicine.medical_specialty, Human immunodeficiency virus (HIV), HIV Infections, medicine.disease_cause, Virus Replication, Gastroenterology, Virus, Article, Pharmacotherapy, Internal medicine, Immunopathology, medicine, Humans, Pharmacology (medical), Sida, Aged, biology, Middle Aged, Viral Load, biology.organism_classification, CD4 Lymphocyte Count, Infectious Diseases, Lentivirus, Immunology, HIV-1, Female, Viral disease, Viral load
Abstract

Objectives: To evaluate the association between baseline (BL) replication capacity (RC) (RC BL ) and immunologic/virologic parameters (at BL and after 48 weeks on therapy) in HIV-1-infected subjects initiating antiretroviral therapy. Methods: RC BL was determined using a modified Monogram PhenoSense HIV drug susceptibility assay on plasma HIV-1 from 321 treatment-naive subjects from AIDS Clinical Trials Group 384. Univariate and multivariable analyses were performed to determine the association of RC BL with BL and on-therapy virologic and immunologic outcomes. Results: Higher RC BL was associated with lower baseline CD4 (CD4 BL ) (r = -0.23, P < 0.0001), higher baseline HIV-1 RNA (r = 0.25, P < 0.0001), higher CD4 BL activation percent (r = 0.23, P < 0.0001), and lower CD4 BL memory count (r = -0.21, P = 0.0002). In a multivariable model, week 48 CD4 increase (ΔCD4 48 ) was associated with lower CD4 BL memory count and higher CD4 BL -naive percent (P = 0.004, P = 0.015, respectively). The interaction between CD4 BL and RC BL was significant (P = 0.018), with a positive association between RC BL and ΔCD4 48 in subjects with higher CD4 BL and a negative association at lower absCD4 BL . Conclusions: At baseline, higher RC was significantly associated with higher HIV-1 RNA, higher CD4 cell activation, lower CD4 cell count, and lower CD4 memory cell count. These factors may interact, directly or indirectly, to modify the extent to which CD4 recovery occurs in patients starting antiretroviral therapy at different CD4 BL counts.

Published
2009

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