Phenotypic characterization of virological failure following lopinavir/ritonavir monotherapy using full-length gag-protease genes

Journal of Antimicrobial Chemotherapy

Volumn 69, Issue 12, 2014, Pages 3340-3348

  Sutherland, Katherine A ^a   Mbisa, Jean L ^a   Ghosn, Jade ^b,c   Chaix, Marie Laure ^b   Cohen Codar, Isabelle ^d   Hue, Stephane ^e   Delfraissy, Jean Francois ^f   Delaugerre, Constance ^b   Gupta, Ravindra K ^e  

^a PUBLIC HEALTH ENGLAND   (United Kingdom)

^b UNIVERSITÉ PARIS DESCARTES   (France)

^c HÔTEL DIEU   (France)

^d ABBVIE INC   (United States)

^e UNIVERSITY COLLEGE LONDON   (United Kingdom)

^f BICÊTRE HOSPITAL   (France)

Author keywords

Antiretroviral resistance; Gag; HIV; Monotherapy; Protease inhibitors

Indexed keywords

ATAZANAVIR; DARUNAVIR; LOPINAVIR; LOPINAVIR PLUS RITONAVIR; SAQUINAVIR; ANTI HUMAN IMMUNODEFICIENCY VIRUS AGENT; GAG PROTEIN; HUMAN IMMUNODEFICIENCY VIRUS PROTEINASE; RITONAVIR;

AMINO ACID SUBSTITUTION; ANTIVIRAL SUSCEPTIBILITY; ARTICLE; CLINICAL ARTICLE; DRUG TREATMENT FAILURE; GAG GENE; GENE; HUMAN; HUMAN IMMUNODEFICIENCY VIRUS INFECTION; MONOTHERAPY; NONHUMAN; PATIENT COMPLIANCE; PHENOTYPE; PHYLOGENY; PROTEASE GENE; VIRUS INFECTIVITY; VIRUS INHIBITION; ANTIVIRAL RESISTANCE; GENETICS; GENOTYPE; HIV INFECTIONS; METABOLISM; MICROBIAL SENSITIVITY TEST; TREATMENT FAILURE;

ANTI-HIV AGENTS; DRUG RESISTANCE, VIRAL; GAG GENE PRODUCTS, HUMAN IMMUNODEFICIENCY VIRUS; GENOTYPE; HIV INFECTIONS; HIV PROTEASE; HUMANS; LOPINAVIR; MICROBIAL SENSITIVITY TESTS; PHENOTYPE; RITONAVIR; TREATMENT FAILURE;

EID: 84928342034     PISSN: 03057453     EISSN: 14602091     Source Type: Journal    
DOI: 10.1093/jac/dku296     Document Type: Article

References (40)

1. Hosseinipour MC, van Oosterhout JJ, Weigel R et al. The public health approach to identify antiretroviral therapy failure: high-level nucleoside reverse transcriptase inhibitor resistance among Malawians failing firstline antiretroviral therapy. AIDS 2009; 23: 1127-34.
2. Gupta RK, Hill A, Sawyer AWet al. Virological monitoring and resistance to first-line highly active antiretroviral therapy in adults infected with HIV-1 treated under WHO guidelines: a systematic review and meta-analysis. Lancet Infect Dis 2009; 9: 409-17.
3. Sungkanuparph S, Manosuthi W, Kiertiburanakul S et al. Options for a second-line antiretroviral regimen for HIV type 1-infected patients whose initial regimen of a fixed-dose combination of stavudine, lamivudine, and nevirapine fails. Clin Infect Dis 2007; 44: 447-52.
4. Hosseinipour MC, Gupta RK, Van Zyl G et al. Emergence of HIVdrug resistance during first-and second-line antiretroviral therapy in resourcelimited settings. J Infect Dis 2013; 207 Suppl 2: S49-56.
5. Messou E, Chaix ML, Gabillard D et al. Increasing rate of TAMs and etravirine resistance in HIV-1-infected adults between 12 and 24 months of treatment: the VOLTART cohort study in Cote d'Ivoire, West Africa. J Acquir Immune Defic Syndr 2013; 64: 211-9.
6. Murphy RA, Sunpath H, Castilla C et al. Second-line antiretroviral therapy: long-term outcomes in South Africa. J Acquir Immune Defic Syndr 2012; 61: 158-63.
7. Ajose O, Mookerjee S, Mills EJ et al. Treatment outcomes of patients on second-line antiretroviral therapy in resource-limited settings: a systematic review and meta-analysis. AIDS 2012; 26: 929-38.
8. Saravanan S, Vidya M, Balakrishnan P et al. Viremia and HIV-1 drug resistance mutations among patients receiving second-line highly active antiretroviral therapy in Chennai, Southern India. Clin Infect Dis 2012; 54: 995-1000.
9. Gilks CF,Walker AS, Dunn DT et al. Lopinavir/ritonavir monotherapy after 24 weeks of second-line antiretroviral therapy in Africa: a randomized controlled trial (SARA). Antivir Ther 2012; 17: 1363-73.
10. Paton NI, Kityo C, Hoppe A et al. Assessment of second-line antiretroviral regimens for HIV therapy in Africa. N Engl J Med 2014; 371: 234-47.
11. Bunupuradah T, Chetchotisakd P, Ananworanich J et al. A randomized comparison of second-line lopinavir/ritonavir monotherapy versus tenofovir/lamivudine/lopinavir/ritonavir in patients failing NNRTI regimens: the HIV STAR study. Antivir Ther 2012; 17: 1351-61.
12. Bartlett JA, Ribaudo HJ,Wallis CL et al. Lopinavir/ritonavir monotherapy after virologic failure of first-line antiretroviral therapy in resource-limited settings. AIDS 2012; 26: 1345-54.
13. Ghosn J, Flandre P, Cohen-Codar I et al. Long-term (96-week) follow-up of antiretroviral-naive HIV-infected patients treated with first-line lopinavir/ritonavir monotherapy in the MONARK trial. HIV Med 2010; 11: 137-42.
14. Delfraissy JF, Flandre P, Delaugerre C et al. Lopinavir/ritonavir monotherapy or plus zidovudine and lamivudine in antiretroviral-naive HIV-infected patients. AIDS 2008; 22: 385-93.
15. Arribas JR, Clumeck N, Nelson M et al. The MONET trial: week 144 analysis of the efficacy of darunavir/ritonavir (DRV/r) monotherapy versus DRV/r plus two nucleoside reverse transcriptase inhibitors, for patients with viral load ,50 HIV-1 RNA copies/mL at baseline. HIV Med 2012; 13: 398-405.
16. Pulido F, Arribas JR, Delgado R et al. Lopinavir-ritonavir monotherapy versus lopinavir-ritonavir and two nucleosides for maintenance therapy of HIV. AIDS 2008; 22: F1-9.
17. Arribas JR, Delgado R, Arranz A et al. Lopinavir-ritonavir monotherapy versus lopinavir-ritonavir and 2 nucleosides for maintenance therapy of HIV: 96-week analysis. J Acquir Immune Defic Syndr 2009; 51: 147-52.
18. Delaugerre C, Flandre P, Chaix ML et al. Protease inhibitor resistance analysis in the MONARK trial comparing first-line lopinavir-ritonavir monotherapy to lopinavir-ritonavir plus zidovudine and lamivudine triple therapy. Antimicrob Agents Chemother 2009; 53: 2934-9.
19. Hill A, McBride A, Sawyer AWet al. Resistance at virological failure using boosted protease inhibitors versus nonnucleoside reverse transcriptase inhibitors as first-line antiretroviral therapy: implications for sustained efficacy of ART in resource-limited settings. J Infect Dis 2013; 207 Suppl 2: S78-84.
20. Gupta R, Hill A, Sawyer AWet al. Emergence of drug resistance in HIV type 1-infected patients after receipt of first-line highly active antiretroviral therapy: a systematic review of clinical trials. Clin Infect Dis 2008; 47: 712-22.
21. Ghosn J, Delaugerre C, Flandre P et al. Polymorphism in Gag gene cleavage sites of HIV-1 non-B subtype and virological outcome of a first-line lopinavir/ritonavir single drug regimen. PLoS One 2011; 6: e24798.
22. Fun A, Wensing AM, Verheyen J et al. Human immunodeficiency virus Gag and protease: partners in resistance. Retrovirology 2012; 9: 63.
23. McKinnon JE, Delgado R, Pulido F et al. Single genome sequencing of HIV-1 gag and protease resistance mutations at virologic failure during the OK04 trial of simplified versus standard maintenance therapy. Antivir Ther 2011; 16: 725-32.
24. Ho SK, Perez EE, Rose SL et al. Genetic determinants in HIV-1 Gag and Env V3 are related to viral response to combination antiretroviral therapy with a protease inhibitor. AIDS 2009; 23: 1631-40.
25. Gupta RK, Kohli A, McCormick AL et al. Full-length HIV-1 Gag determines protease inhibitor susceptibility within in vitro assays. AIDS 2010; 24: 1651-5.
26. Sutherland KA, Mbisa JL, Cane PA et al. Contribution of Gag and protease to variation in susceptibility to protease inhibitors between different strains of subtype B HIV-1. J Gen Virol 2014; 95: 190-200.
27. Parry CM, Kohli A, Boinett CJ et al. Gag determinants of fitness and drug susceptibility in protease inhibitor-resistant human immunodeficiency virus type 1. J Virol 2009; 83: 9094-101.
28. Van Laethem K, Schrooten Y, Dedecker S et al. A genotypic assay for the amplification and sequencing of gag and protease from diverse human immunodeficiency virus type 1 group M subtypes. J Virol Methods 2006; 132: 181-6.
29. Parry CM, Kolli M, Myers RE et al. Three residues in HIV-1 matrix contribute to protease inhibitor susceptibility and replication capacity. Antimicrob Agents Chemother 2011; 55: 1106-13.
30. Tamura K, Peterson D, Peterson N et al. MEGA5: molecular evolutionary genetics analysis using maximum likelihood, evolutionary distance, and maximum parsimony methods. Mol Biol Evol 2011; 28: 2731-9.
31. Guindon S, Dufayard JF, Lefort V et al. New algorithms and methods to estimate maximum-likelihood phylogenies: assessing the performance of PhyML 3.0. Syst Biol 2010; 59: 307-21.
32. de Oliveira T, Deforche K, Cassol S et al. An automated genotyping system for analysis of HIV-1 and other microbial sequences. Bioinformatics 2005; 21: 3797-800.
33. Alcantara LC, Cassol S, Libin P et al. A standardized framework for accurate, high-throughput genotyping of recombinant and nonrecombinant viral sequences. Nucl Acids Res 2009; 37: W634-42.
34. Aoki M, Venzon DJ, Koh Y et al. Non-cleavage site gag mutations in amprenavir-resistant human immunodeficiency virus type 1 (HIV-1) predispose HIV-1 to rapid acquisition of amprenavir resistance but delay development of resistance to other protease inhibitors. J Virol 2009; 83: 3059-68.
35. King MS, Rode R, Cohen-Codar I et al. Predictive genotypic algorithmfor virologic response to lopinavir-ritonavir in protease inhibitor-experienced patients. Antimicrob Agents Chemother 2007; 51: 3067-74.
36. Santos JR, Llibre JM, Imaz A et al. Mutations in the protease gene associated with virological failure to lopinavir/ritonavir-containing regimens. J Antimicrob Chemother 2012; 67: 1462-9.
37. Kempf DJ, King MS, Bernstein B et al. Incidence of resistance in a double-blind study comparing lopinavir/ritonavir plus stavudine and lamivudine to nelfinavir plus stavudine and lamivudine. J Infect Dis 2004; 189: 51-60.
38. Kempf DJ, Isaacson JD, King MS et al. Identification of genotypic changes in human immunodeficiency virus protease that correlate with reduced susceptibility to the protease inhibitor lopinavir among viral isolates from protease inhibitor-experienced patients. J Virol 2001; 75: 7462-9.
39. Johnson VA, Calvez V, Gunthard HF et al. Update of the Drug Resistance Mutations in HIV-1: March 2013. http://www.iasusa.org/sites/default/files/tam/21-1-6.pdf.
40. Rabi SA, Laird GM, Durand CM et al. Multi-step inhibition explains HIV-1 protease inhibitor pharmacodynamics and resistance. J Clin Invest 2013; 123: 3848-60.