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      Current Perspectives on HIV-1 Antiretroviral Drug Resistance

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      Author(s): , *
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      Publication date (Electronic):
      Journal: Viruses
      Publisher: MDPI
      Keywords: HIV-1, antiviral therapy, drug resistance, evolution, lethal mutagenesis, resistance monitoring

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          Abstract

          Current advancements in antiretroviral therapy (ART) have turned HIV-1 infection into a chronic and manageable disease. However, treatment is only effective until HIV-1 develops resistance against the administered drugs. The most recent antiretroviral drugs have become superior at delaying the evolution of acquired drug resistance. In this review, the viral fitness and its correlation to HIV-1 mutation rates and drug resistance are discussed while emphasizing the concept of lethal mutagenesis as an alternative therapy. The development of resistance to the different classes of approved drugs and the importance of monitoring antiretroviral drug resistance are also summarized briefly.

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          Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection.

          D Ho, A Neumann, A S Perelson … (1995)
          Treatment of infected patients with ABT-538, an inhibitor of the protease of human immunodeficiency virus type 1 (HIV-1), causes plasma HIV-1 levels to decrease exponentially (mean half-life, 2.1 +/- 0.4 days) and CD4 lymphocyte counts to rise substantially. Minimum estimates of HIV-1 production and clearance and of CD4 lymphocyte turnover indicate that replication of HIV-1 in vivo is continuous and highly productive, driving the rapid turnover of CD4 lymphocytes.
          Article 0 comments Cited 547 times – based on 0 reviews     Review now
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            Quantification of latent tissue reservoirs and total body viral load in HIV-1 infection.

            Tae-Wook Chun, Lucy Carruth, Diana Finzi … (1997)
            The capacity of HIV-1 to establish latent infection of CD4+ T cells may allow viral persistence despite immune responses and antiretroviral therapy. Measurements of infectious virus and viral RNA in plasma and of infectious virus, viral DNA and viral messenger RNA species in infected cells all suggest that HIV-1 replication continues throughout the course of infection. Uncertainty remains over what fraction of CD4+ T cells are infected and whether there are latent reservoirs for the virus. We show here that during the asymptomatic phase of infection there is an extremely low total body load of latently infected resting CD4+ T cells with replication-competent integrated provirus (<10(7) cells). The most prevalent form of HIV-1 DNA in resting and activated CD4+ T cells is a full-length, linear, unintegrated form that is not replication competent. The infection progresses even though at any given time in the lymphoid tissues integrated HIV-1 DNA is present in only a minute fraction of the susceptible populations, including resting and activated CD4+ T cells and macrophages.
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              HIV-1 dynamics in vivo: virion clearance rate, infected cell life-span, and viral generation time.

              Victor Markowitz, Alan Perelson, Anthony Ho … (1996)
              A new mathematical model was used to analyze a detailed set of human immunodeficiency virus-type 1 (HIV-1) viral load data collected from five infected individuals after the administration of a potent inhibitor of HIV-1 protease. Productively infected cells were estimated to have, on average, a life-span of 2.2 days (half-life t 1/2 = 1.6 days), and plasma virions were estimated to have a mean life-span of 0.3 days (t 1/2 = 0.24 days). The estimated average total HIV-1 production was 10.3 x 10(9) virions per day, which is substantially greater than previous minimum estimates. The results also suggest that the minimum duration of the HIV-1 life cycle in vivo is 1.2 days on average, and that the average HIV-1 generation time--defined as the time from release of a virion until it infects another cell and causes the release of a new generation of viral particles--is 2.6 days. These findings on viral dynamics provide not only a kinetic picture of HIV-1 pathogenesis, but also theoretical principles to guide the development of treatment strategies.
              Article 0 comments Cited 305 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Eric O. Freed: Role: External Editor
                Journal
                Journal ID (nlm-ta): Viruses
                Journal ID (iso-abbrev): Viruses
                Journal ID (publisher-id): viruses
                Title: Viruses
                Publisher: MDPI
                ISSN (Electronic): 1999-4915
                Publication date (Electronic): 24 October 2014
                Publication date Collection: October 2014
                Volume: 6
                Issue: 10
                Pages: 4095-4139
                Affiliations
                Department of Pharmacology, School of Medicine, Yale University, New Haven, CT 06520, USA; E-Mail: pinar.iyidogan@ 123456yale.edu
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: karen.anderson@ 123456yale.edu ; Tel.: +1-203-785-4526; Fax: +1-203-785-7670.
                Article
                Publisher ID: viruses-06-04095
                DOI: 10.3390/v6104095
                PMC ID: 4213579
                PubMed ID: 25341668
                SO-VID: 97edbd06-9ae8-4edb-bdb8-880c35b985a3
                Copyright © © 2014 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 28 July 2014
                Date revision received : 08 October 2014
                Date accepted : 20 October 2014
                Categories
                Subject: Review

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: hiv-1,antiviral therapy,drug resistance,evolution,lethal mutagenesis,resistance monitoring
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: hiv-1, antiviral therapy, drug resistance, evolution, lethal mutagenesis, resistance monitoring

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