Show simple item record Asmuth, DM Murphy, RL Rosenkranz, SL Lertora, JJ Kottilil, S Cramer, Y Chan, ES Schooley, RT Rinaldo, CR Thielman, N Li, XD Wahl, SM Shore, J Janik, J Lempicki, RA Simpson, Y Pollard, RB AIDS Clinical Trials Group A5192 Team
dc.coverage.spatial United States 2011-06-21T17:27:21Z 2010-06-01
dc.identifier.citation J Infect Dis, 2010, 201 (11), pp. 1686 - 1696
dc.description.abstract BACKGROUND: To our knowledge, the antiviral activity of pegylated interferon alfa-2a has not been studied in participants with untreated human immunodeficiency virus type 1 (HIV-1) infection but without chronic hepatitis C virus (HCV) infection. METHODS: Untreated HIV-1-infected volunteers without HCV infection received 180 microg of pegylated interferon alfa-2a weekly for 12 weeks. Changes in plasma HIV-1 RNA load, CD4(+) T cell counts, pharmacokinetics, pharmacodynamic measurements of 2',5'-oligoadenylate synthetase (OAS) activity, and induction levels of interferon-inducible genes (IFIGs) were measured. Nonparametric statistical analysis was performed. RESULTS: Eleven participants completed 12 weeks of therapy. The median plasma viral load decrease and change in CD4(+) T cell counts at week 12 were 0.61 log(10) copies/mL (90% confidence interval [CI], 0.20-1.18 log(10) copies/mL) and -44 cells/microL (90% CI, -95 to 85 cells/microL), respectively. There was no correlation between plasma viral load decreases and concurrent pegylated interferon plasma concentrations. However, participants with larger increases in OAS level exhibited greater decreases in plasma viral load at weeks 1 and 2 (r = -0.75 [90% CI, -0.93 to -0.28] and r = -0.61 [90% CI, -0.87 to -0.09], respectively; estimated Spearman rank correlation). Participants with higher baseline IFIG levels had smaller week 12 decreases in plasma viral load (0.66 log(10) copies/mL [90% CI, 0.06-0.91 log(10) copies/mL]), whereas those with larger IFIG induction levels exhibited larger decreases in plasma viral load (-0.74 log(10) copies/mL [90% CI, -0.93 to -0.21 log(10) copies/mL]). CONCLUSION: Pegylated interferon alfa-2a was well tolerated and exhibited statistically significant anti-HIV-1 activity in HIV-1-monoinfected patients. The anti-HIV-1 effect correlated with OAS protein levels (weeks 1 and 2) and IFIG induction levels (week 12) but not with pegylated interferon concentrations.
dc.format.extent 1686 - 1696
dc.language eng
dc.language.iso en_US en_US
dc.relation.ispartof J Infect Dis
dc.relation.isversionof 10.1086/652420
dc.subject 2',5'-Oligoadenylate Synthetase
dc.subject Adult
dc.subject Anti-HIV Agents
dc.subject CD4 Lymphocyte Count
dc.subject Gene Expression Profiling
dc.subject HIV Infections
dc.subject HIV-1
dc.subject Humans
dc.subject Interferon-alpha
dc.subject Male
dc.subject Middle Aged
dc.subject Polyethylene Glycols
dc.subject RNA, Viral
dc.subject Recombinant Proteins
dc.subject Treatment Outcome
dc.subject Viral Load
dc.title Safety, tolerability, and mechanisms of antiretroviral activity of pegylated interferon Alfa-2a in HIV-1-monoinfected participants: a phase II clinical trial.
dc.title.alternative en_US
dc.type Journal Article
dc.description.version Version of Record en_US 2010-6-1 en_US
duke.description.endpage 1696 en_US
duke.description.issue 11 en_US
duke.description.startpage 1686 en_US
duke.description.volume 201 en_US
dc.relation.journal Journal of Infectious Diseases en_US
pubs.issue 11
pubs.organisational-group /Duke
pubs.organisational-group /Duke/Institutes and Provost's Academic Units
pubs.organisational-group /Duke/Institutes and Provost's Academic Units/University Institutes and Centers
pubs.organisational-group /Duke/Institutes and Provost's Academic Units/University Institutes and Centers/Global Health Institute
pubs.organisational-group /Duke/School of Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine/Medicine, Infectious Diseases
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Pathology
pubs.publication-status Published
pubs.volume 201
dc.identifier.eissn 1537-6613

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