HIV-1 replication and immune dynamics are affected by raltegravir intensification of HAART-suppressed subjects
Despite highly active antiretroviral therapy, active replication persists and drives immune activation in some individuals with HIV. This activation is higher if therapy is intensified by additional antiretroviral drugs ( pages 373–374 ). Highly active antiretroviral therapy (HAART) results in poten...
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| Published in | Nature medicine Vol. 16; no. 4; pp. 460 - 465 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.04.2010
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Despite highly active antiretroviral therapy, active replication persists and drives immune activation in some individuals with HIV. This activation is higher if therapy is intensified by additional antiretroviral drugs (
pages 373–374
).
Highly active antiretroviral therapy (HAART) results in potent and durable suppression of HIV-1 viremia. However, HIV-1 replication resumes if therapy is interrupted
1
,
2
. Although it is generally believed that active replication has been halted in individuals on HAART, immune activation and inflammation continue at abnormal levels
3
, suggesting continued, low-level viral replication. To assess whether active replication might be driving immune activation in HAART, we examined the impact of treatment intensification with the integrase inhibitor raltegravir on viral complementary DNA and immune activation parameters. In the presence of raltegravir, linear HIV-1 cDNA is prevented from integrating into chromatin and is subsequently converted to episomal cDNAs
4
,
5
. Raltegravir intensification of a three-drug suppressive HAART regimen resulted in a specific and transient increase in episomal DNAs in a large percentage of HAART-suppressed subjects. Furthermore, in subjects with these episomal DNAs, immune activation was higher at baseline and was subsequently normalized after raltegravir intensification. These results suggest that, despite suppressive HAART, active replication persists in some infected individuals and drives immune activation. The ability of raltegravir intensification to perturb the reservoir that supports active replication has implications for therapeutic strategies aimed at achieving viral eradication. |
|---|---|
| AbstractList | Despite highly active antiretroviral therapy, active replication persists and drives immune activation in some individuals with HIV. This activation is higher if therapy is intensified by additional antiretroviral drugs (
pages 373–374
).
Highly active antiretroviral therapy (HAART) results in potent and durable suppression of HIV-1 viremia. However, HIV-1 replication resumes if therapy is interrupted
1
,
2
. Although it is generally believed that active replication has been halted in individuals on HAART, immune activation and inflammation continue at abnormal levels
3
, suggesting continued, low-level viral replication. To assess whether active replication might be driving immune activation in HAART, we examined the impact of treatment intensification with the integrase inhibitor raltegravir on viral complementary DNA and immune activation parameters. In the presence of raltegravir, linear HIV-1 cDNA is prevented from integrating into chromatin and is subsequently converted to episomal cDNAs
4
,
5
. Raltegravir intensification of a three-drug suppressive HAART regimen resulted in a specific and transient increase in episomal DNAs in a large percentage of HAART-suppressed subjects. Furthermore, in subjects with these episomal DNAs, immune activation was higher at baseline and was subsequently normalized after raltegravir intensification. These results suggest that, despite suppressive HAART, active replication persists in some infected individuals and drives immune activation. The ability of raltegravir intensification to perturb the reservoir that supports active replication has implications for therapeutic strategies aimed at achieving viral eradication. Highly active antiretroviral therapy (HAART) results in potent and durable suppression of HIV-1 viremia. However, HIV-1 replication resumes if therapy is interrupted. Although it is generally believed that active replication has been halted in individuals on HAART, immune activation and inflammation continue at abnormal levels, suggesting continued, low-level viral replication. To assess whether active replication might be driving immune activation in HAART, we examined the impact of treatment intensification with the integrase inhibitor raltegravir on viral complementary DNA and immune activation parameters. In the presence of raltegravir, linear HIV-1 cDNA is prevented from integrating into chromatin and is subsequently converted to episomal cDNAs. Raltegravir intensification of a three-drug suppressive HAART regimen resulted in a specific and transient increase in episomal DNAs in a large percentage of HAART-suppressed subjects. Furthermore, in subjects with these episomal DNAs, immune activation was higher at baseline and was subsequently normalized after raltegravir intensification. These results suggest that, despite suppressive HAART, active replication persists in some infected individuals and drives immune activation. The ability of raltegravir intensification to perturb the reservoir that supports active replication has implications for therapeutic strategies aimed at achieving viral eradication. Highly active antiretroviral therapy (HAART) results in potent and durable suppression of HIV-1 viremia. However, HIV-1 replication resumes if therapy is interrupted (1,2). Although it is generally believed that active replication has been halted in individuals on HAART, immune activation and inflammation continue at abnormal levels (3), suggesting continued, low-level viral replication. To assess whether active replication might be driving immune activation in HAART, we examined the impact of treatment intensification with the integrase inhibitor raltegravir on viral complementary DNA and immune activation parameters. In the presence of raltegravir, linear HIV-1 cDNA is prevented from integrating into chromatin and is subsequently converted to episomal cDNAs (4,5). Raltegravir intensification of a three-drug suppressive HAART regimen resulted in a specific and transient increase in episomal DNAs in a large percentage of HAART-suppressed subjects. Furthermore, in subjects with these episomal DNAs, immune activation was higher at baseline and was subsequently normalized after raltegravir intensification. These results suggest that, despite suppressive HAART, active replication persists in some infected individuals and drives immune activation. The ability of raltegravir intensification to perturb the reservoir that supports active replication has implications for therapeutic strategies aimed at achieving viral eradication. Highly active antiretroviral therapy (HAART) results in potent and durable suppression of HIV-1 viremia. However, HIV-1 replication resumes if therapy is interrupted. Although it is generally believed that active replication has been halted in individuals on HAART, immune activation and inflammation continue at abnormal levels, suggesting continued, low-level viral replication. To assess whether active replication might be driving immune activation in HAART, we examined the impact of treatment intensification with the integrase inhibitor raltegravir on viral complementary DNA and immune activation parameters. In the presence of raltegravir, linear HIV-1 cDNA is prevented from integrating into chromatin and is subsequently converted to episomal cDNAs. Raltegravir intensification of a three-drug suppressive HAART regimen resulted in a specific and transient increase in episomal DNAs in a large percentage of HAART-suppressed subjects. Furthermore, in subjects with these episomal DNAs, immune activation was higher at baseline and was subsequently normalized after raltegravir intensification. These results suggest that, despite suppressive HAART, active replication persists in some infected individuals and drives immune activation. The ability of raltegravir intensification to perturb the reservoir that supports active replication has implications for therapeutic strategies aimed at achieving viral eradication. [PUBLICATION ABSTRACT] Highly active antiretroviral therapy (HAART) results in potent and durable suppression of HIV-1 viremia. However, HIV-1 replication resumes if therapy is interrupted. Although it is generally believed that active replication has been halted in individuals on HAART, immune activation and inflammation continue at abnormal levels, suggesting continued, low-level viral replication. To assess whether active replication might be driving immune activation in HAART, we examined the impact of treatment intensification with the integrase inhibitor raltegravir on viral complementary DNA and immune activation parameters. In the presence of raltegravir, linear HIV-1 cDNA is prevented from integrating into chromatin and is subsequently converted to episomal cDNAs. Raltegravir intensification of a three-drug suppressive HAART regimen resulted in a specific and transient increase in episomal DNAs in a large percentage of HAART-suppressed subjects. Furthermore, in subjects with these episomal DNAs, immune activation was higher at baseline and was subsequently normalized after raltegravir intensification. These results suggest that, despite suppressive HAART, active replication persists in some infected individuals and drives immune activation. The ability of raltegravir intensification to perturb the reservoir that supports active replication has implications for therapeutic strategies aimed at achieving viral eradication.Highly active antiretroviral therapy (HAART) results in potent and durable suppression of HIV-1 viremia. However, HIV-1 replication resumes if therapy is interrupted. Although it is generally believed that active replication has been halted in individuals on HAART, immune activation and inflammation continue at abnormal levels, suggesting continued, low-level viral replication. To assess whether active replication might be driving immune activation in HAART, we examined the impact of treatment intensification with the integrase inhibitor raltegravir on viral complementary DNA and immune activation parameters. In the presence of raltegravir, linear HIV-1 cDNA is prevented from integrating into chromatin and is subsequently converted to episomal cDNAs. Raltegravir intensification of a three-drug suppressive HAART regimen resulted in a specific and transient increase in episomal DNAs in a large percentage of HAART-suppressed subjects. Furthermore, in subjects with these episomal DNAs, immune activation was higher at baseline and was subsequently normalized after raltegravir intensification. These results suggest that, despite suppressive HAART, active replication persists in some infected individuals and drives immune activation. The ability of raltegravir intensification to perturb the reservoir that supports active replication has implications for therapeutic strategies aimed at achieving viral eradication. |
| Audience | Academic |
| Author | Blanco, Julià Stevenson, Mario Martinez-Picado, Javier J Buzón, Maria Palmer, Sarah Clotet, Bonaventura Domingo, Pere Llibre, Josep M Puertas, Maria C Massanella, Marta Gatell, Josep M Paredes, Roger Dahl, Viktor Sharkey, Mark Esteve, Anna |
| Author_xml | – sequence: 1 givenname: Maria surname: J Buzón fullname: J Buzón, Maria organization: irsiCaixa Foundation, Institut Germans Trias i Pujol, Universitat Autònoma de Barcelona – sequence: 2 givenname: Marta surname: Massanella fullname: Massanella, Marta organization: irsiCaixa Foundation, Institut Germans Trias i Pujol, Universitat Autònoma de Barcelona – sequence: 3 givenname: Josep M surname: Llibre fullname: Llibre, Josep M organization: 'Lluita contra la SIDA' Foundation – sequence: 4 givenname: Anna surname: Esteve fullname: Esteve, Anna organization: Center for Epidemiological Studies on STI and HIV/AIDS of Catalonia – sequence: 5 givenname: Viktor surname: Dahl fullname: Dahl, Viktor organization: Swedish Institute for Infectious Disease Control – sequence: 6 givenname: Maria C surname: Puertas fullname: Puertas, Maria C organization: irsiCaixa Foundation, Institut Germans Trias i Pujol, Universitat Autònoma de Barcelona – sequence: 7 givenname: Josep M surname: Gatell fullname: Gatell, Josep M organization: Hospital Clínic-Idibaps – sequence: 8 givenname: Pere surname: Domingo fullname: Domingo, Pere organization: Hospital Sant Pau – sequence: 9 givenname: Roger surname: Paredes fullname: Paredes, Roger organization: irsiCaixa Foundation, Institut Germans Trias i Pujol, Universitat Autònoma de Barcelona, 'Lluita contra la SIDA' Foundation – sequence: 10 givenname: Mark surname: Sharkey fullname: Sharkey, Mark organization: University of Massachusetts Medical School – sequence: 11 givenname: Sarah surname: Palmer fullname: Palmer, Sarah organization: Swedish Institute for Infectious Disease Control – sequence: 12 givenname: Mario surname: Stevenson fullname: Stevenson, Mario organization: University of Massachusetts Medical School – sequence: 13 givenname: Bonaventura surname: Clotet fullname: Clotet, Bonaventura organization: irsiCaixa Foundation, Institut Germans Trias i Pujol, Universitat Autònoma de Barcelona, 'Lluita contra la SIDA' Foundation – sequence: 14 givenname: Julià surname: Blanco fullname: Blanco, Julià organization: irsiCaixa Foundation, Institut Germans Trias i Pujol, Universitat Autònoma de Barcelona – sequence: 15 givenname: Javier surname: Martinez-Picado fullname: Martinez-Picado, Javier email: jmpicado@irsicaixa.es organization: irsiCaixa Foundation, Institut Germans Trias i Pujol, Universitat Autònoma de Barcelona, Catalan Institution for Research and Advanced Studies |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20228817$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:120281249$$DView record from Swedish Publication Index |
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| Snippet | Despite highly active antiretroviral therapy, active replication persists and drives immune activation in some individuals with HIV. This activation is higher... Highly active antiretroviral therapy (HAART) results in potent and durable suppression of HIV-1 viremia. However, HIV-1 replication resumes if therapy is... |
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| SubjectTerms | 631/326/596/1296 631/92/436/2388 692/699/249/1570/1901 Antiretroviral agents Antiretroviral Therapy, Highly Active Antiviral drugs Biomedical and Life Sciences Biomedicine Cancer Research Deoxyribonucleic acid DNA DNA, Complementary - genetics DNA, Viral - genetics Dosage and administration Drug therapy Health aspects Highly active antiretroviral therapy HIV HIV infection HIV Infections - drug therapy HIV Infections - immunology HIV Infections - virology HIV Integrase Inhibitors - pharmacology HIV Integrase Inhibitors - therapeutic use HIV Long Terminal Repeat - drug effects HIV Long Terminal Repeat - genetics HIV-1 - drug effects HIV-1 - immunology HIV-1 - physiology Human immunodeficiency virus Human immunodeficiency virus 1 Humans Immunology Infectious Diseases Inhibitor drugs letter Metabolic Diseases Molecular Medicine Neurosciences Polymerase Chain Reaction Pyrrolidinones - pharmacology Pyrrolidinones - therapeutic use Raltegravir Raltegravir Potassium Virus Integration - drug effects Virus Replication - drug effects Virus Replication - physiology |
| Title | HIV-1 replication and immune dynamics are affected by raltegravir intensification of HAART-suppressed subjects |
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