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Attacking latent HIV provirus: from mechanism to therapeutic strategies

Attacking latent HIV provirus: from mechanism to therapeutic strategies Attacking latent HIV provirus: from mechanism to therapeutic strategies a a,b,c Nancy M. Archin and David M. Margolis Purpose of review Abbreviations The persistence of small population integrated proviral HIV HAART highly active antiretroviral therapy HDAC histone deacetylase genomes capable of expressing HIV within long-lived CD4 LSF late-specific transcription factor T cells is a fundamental obstacle to the eradication or cure LTR long-terminal repeat PKC protein kinase C of HIV infection. As potent antiretroviral therapy by itself VPA valproic acid appears to be an impractical approach to the eradication of this quiescent reservoir of HIV infection, new approaches 2006 Lippincott Williams & Wilkins are required. 1746-630X Recent findings Initial studies failed to demonstrate that simultaneous, intensive antiretroviral therapy in combination with global Introduction inducers of CD4 T-cell activation could eradicate HIV The HIV pandemic is now more than 20 years old. Over infection. Global T-cell activation may induce viral 40 million people are infected worldwide, with millions in replication and increase the number of susceptible need antiretroviral therapy [1,2]. Even in the United uninfected target cells beyond the threshold that can be States where the incidence of infection is rising only contained by current antiretroviral therapy. Future advances modestly, http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Opinion in HIV and Aids Wolters Kluwer Health

Attacking latent HIV provirus: from mechanism to therapeutic strategies

Current Opinion in HIV and Aids , Volume 1 (2) – Mar 1, 2006

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References (78)

ISSN
1746-630X
eISSN
1746-6318
DOI
10.1097/01.COH.0000203837.47092.fd
pmid
19372797
Publisher site
See Article on Publisher Site

Abstract

Attacking latent HIV provirus: from mechanism to therapeutic strategies a a,b,c Nancy M. Archin and David M. Margolis Purpose of review Abbreviations The persistence of small population integrated proviral HIV HAART highly active antiretroviral therapy HDAC histone deacetylase genomes capable of expressing HIV within long-lived CD4 LSF late-specific transcription factor T cells is a fundamental obstacle to the eradication or cure LTR long-terminal repeat PKC protein kinase C of HIV infection. As potent antiretroviral therapy by itself VPA valproic acid appears to be an impractical approach to the eradication of this quiescent reservoir of HIV infection, new approaches 2006 Lippincott Williams & Wilkins are required. 1746-630X Recent findings Initial studies failed to demonstrate that simultaneous, intensive antiretroviral therapy in combination with global Introduction inducers of CD4 T-cell activation could eradicate HIV The HIV pandemic is now more than 20 years old. Over infection. Global T-cell activation may induce viral 40 million people are infected worldwide, with millions in replication and increase the number of susceptible need antiretroviral therapy [1,2]. Even in the United uninfected target cells beyond the threshold that can be States where the incidence of infection is rising only contained by current antiretroviral therapy. Future advances modestly,

Journal

Current Opinion in HIV and AidsWolters Kluwer Health

Published: Mar 1, 2006

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