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2014, Number 3

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Rev Med MD 2014; 5.6 (3)

New antiretroviral therapies in HIV infection

González-Hernández LA, Llamas-Covarrubias MA, González-Vázquez EA, Campos-Loza AE, Arce-Rosas JI, Mercado-Nuñez E, Soria-Rodríguez R, García-Castro JA, Andrade-Villanueva JF

Language: Spanish
References: 21
Page: 143-149
PDF size: 1068.46 Kb.


ABSTRACT

There are about 34 million people living with Human Immunodeficiency Virus (HIV), and for them the best hope to prevent a lethal infection lays in antiretroviral therapy (ARV), which consists in a combination of three drugs that inhibit specific points of the viral life cycle. The benefits in reducing morbidity and mortality conferred by antiretroviral therapy are quite obvious, however cure is not one of them, due to the fact that there are cells infected in a latent form, called reservoirs that make it impossible to eradicate infection. Antiretroviral therapy has effectively changed the natural history of infection by human immunodeficiency virus. Currently there are over 20 antiretroviral drugs in the market approved by the Food and Drug Administration. Even so, due to the emergence of resistant strains new drugs are in development in order to offer new alternatives to patients requiring them.


REFERENCES

  1. 1.A. Zolopa, R Ortiz, P. Sax, et al. Comparative Study of Tenofovir Alafenamide vs Tenofovir Disoproxil Fumarate, Each with Elvitegravir, Cobicistat, and Emtricitabine, for HIV Treatment. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, GA, March 3-6, 2013. Abstract 99LB.

  2. 2.Rujuta Bam, S Yant, and T Cihlar. Tenofovir Alafenamide (GS-7340) Is Not a Substrate for Renal Organic Anion Transporters (OAT) and Does Not Exhibit OAT-dependent Cytotoxicity. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, GA, March 3-6, 2013. Abstract 540.

  3. 3.Saag MS. New and Investigational Antiretroviral Drugs for HIV Infection: Mechanisms of Action and Early Research Findings. Top Antivir Med. 2012 Dec;20(5):162-7. 4.Anderson M, Gilmarti J, Robberechts M, et al. Safety and Antiviral Activity of MK-1439, a Novel NNRTI, in Treatment-naive HIV+ Patients. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, March 3-6, 2013. Abstract 100.

  4. 5.Anderson M, Gilmarti J, Robberechts M, et al. Safety, Tolerability, and Pharmacokinetics of Single and Multiple Doses of MK-1439, a Novel HIV NNRTI, in Healthy Subjects. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, March 3-6, 2013. Abstract 527.

  5. 6.Lai M, Feng M, Lu M, et al. Antiviral activity and in vitro mutation development pathways of MK-1439: a novel non-nucleoside reverse transcriptase inhibitor. 52nd Interscience Conference on Antimicrobials and Chemotherapy (ICAAC). September 9-12, 2012. San Francisco. Abstract H-551.

  6. 7.Ferris AL, 2009. Lens epthelium-derived growth factor fusion proteins redirect HIV-1 DNA integration. PNAS 107:3135-3140.

  7. 8.B Desimmie, Frauke Christ, W Thys, J Demeulemeester, D Borrenberghs, R Schrijvers, J Hofkens, N Bannert, and Z Debyser. Viral Particles Produced in Presence of LEDGIN Are Impaired for Infectivity. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, GA, March 3-6, 2013. Abstract 104.

  8. 9.Christ F, Voet A, Marchand A, et al. First-in-class Inhibitors of LEDGF/p75-integrase Interaction and HIV replication. 17th Conference on Retroviruses & Opportunistic Infections (CROI 2010). San Francisco. February 16-19, 2010. Abstract 49.

  9. 10.E Le Rouzic, D Bonnard, S Chasset, J-M Bruneau, F Chevreuil, F Le Strat, S Emiliani, B Ledoussal, F Moreau, and Richard Benarous. Mut101 Integrase- LEDGF Inhibitor Impairs HIV-1 Replication at Two Different Steps, Integration and Production of Infectious Virions after Integration. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, March 3-6, 2013. Abstract 547.

  10. 11.Stephen Yant, L Tsai, C O'Sullivan, T Cihlar, and M Balakrishnan. Non-Catalytic Site Integrase Inhibitors Target the Integrase Domain during Virus Production and Induce a Reverse Transcription Block. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, GA, March 3-6, 2013. Abstract 103.

  11. 12.Lalezari, McCallister S, Gigliotti M, et al. A phase 2 safety and efficacy study of bevirimat in heavily treatment experienced HIV+ patients identifies the target phase 3 study profile. 48th Annual International Conference on Antimicrobial Agents and Chemotherapy (ICAAC). October 25-28, 2008. Washington, DC. Abstract H-891.

  12. 13.E Urano, S Ablan, D Martin, T Nitz, E Freed, and Carl Wild. Potent Antiviral Activity of 2nd Generation Maturation Inhibitors Against Bevirimatresistant Polymorphic HIV-1 Isolates. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, March 3-6, 2013. Abstract 105.

  13. 14.Gathe J, Cade J, DeJesus E, et al. Week-24 Primary Analysis of Cenicriviroc vs Efavirenz, in Combination with Emtricitabine/Tenofovir, in Treatment-naïve HIV-1+ Adults with CCR5-tropic Virus. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, March 3-6, 2013. Abstract 106LB.

  14. 15.Nowicka-Sans B, et al. Antiviral Activity of a New Small Molecule HIV-1 Attachment Inhibitor, BMS- 626529, the Parent of BMS-663068. 18th Conference on Retroviruses and Opportunistic Infections, abstract 518, Boston, 2011.

  15. 16.Nettles R, et al. Pharmacodynamics, Safety, and Pharmacokinetics of BMS-663068: A Potentially First-in-class Oral HIV Attachment Inhibitor. 18th Conference on Retroviruses and Opportunistic Infections, abstract 49, Boston, 2011.

  16. 17.David Langley, R Kimura, P Sivaprakasam, N Zhou, I Dicker, T Wang, J Kadow, N Meanwell, and M Krystal. Homology Models of the Attachment Inhibitor BMS-626529 Bound to gp120 Suggests a Unique Mechanism of Action. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, March 3-6, 2013. Abstract 542.

  17. 18.L Zhu, C Hwang, V Shah, M Hruska, P Hu, B Vakkalagadda, M Furlong, X Xu, G Hanna, and Richard Bertz. Pharmacokinetic Interactions Between BMS-663068, Prodrug of the HIV-1 Attachment Inhibitor BMS-626529, and Ritonavir or Ritonavir-boosted Atazanavir. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, March 3-6, 2013. Abstract 534.

  18. 19.Z. Li, N. Zhou1, Y. Sun, N. Ray, M. Lataillade, G. Hanna, M. Krystal. Activity of the HIV-1 attachment inhibitor BMS-626529 against HIV-1 envelopes resistant to other entry inhibitors. XIX International AIDS Conference, Washington DC, USA. July 22-27, 2012. Abstract TUPE015.

  19. 20.Raffi F, Rachlis A, Stellbrink HJ, et al. Once-daily dolutegravir (DTG; S/GSK1349572) is non-inferior to raltegravir (RAL) in antiretroviral naive adults: 48 week results from SPRING-2 (ING113086). XIX International AIDS Conference. Washington, DC, July 22-27, 2012.

  20. 21.Pozniak A, Mingrone H, Shuldyakov A, et al. Dolutegravir vs raltegravir in ART-experienced, integrase-naive subjects: 24-week interim results from SAILING (ING111762). 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, March 3-6, 2013. Abstract 179LB.

  21. 22.Chasity Andrews, A Gettie1, K Russell-Lodrigue, L Moss, H Mohri1, W Spreen, C Cheng-Mayer, Z Hong, M Markowitz, and D Ho. Long-acting Parenteral Formulation of GSK1265744 Protects Macaques against Repeated Intrarectal Challenges with SHIV. 20th Conference on Retroviruses and Opportunistic Infections. Atlanta, March 3-6, 2013. Abstract 24LB.




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