Virological rebound after suppression on highly active antiretroviral therapy

被引:89
作者
Mocroft, A
Ruiz, L
Reiss, P
Ledergerber, B
Katlama, C
Lazzarin, A
Goebel, FD
Phillips, AN
Clotet, B
Lundgren, JD
机构
[1] UCL Royal Free & UCL Med Sch, Royal Free Ctr HIV Med, London NW3 2PF, England
[2] UCL Royal Free & UCL Med Sch, Dept Primary Care & Populat Sci, London NW3 2PF, England
[3] Hosp Univ UAB Germans Trias & Pujol, Fundacio IrsiCaixa, Badalona, Spain
[4] Hosp Univ UAB Germans Trias & Pujol, HIV Unit, Badalona, Spain
[5] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands
[6] Univ Zurich Hosp, CH-8091 Zurich, Switzerland
[7] Hop La Pitie Salpetriere, Paris, France
[8] Univ Milan, Osped San Raffaele, I-20127 Milan, Italy
[9] Univ Munich, Med Poliklin, D-8000 Munich, Germany
[10] Univ Copenhagen, Hvidovre Hosp, CHIP, DK-2650 Hvidovre, Denmark
关键词
highly active antiretroviral therapy; rebound; response; viral load;
D O I
10.1097/00002030-200308150-00003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Objective: To determine the rate of virological rebound and factors associated with rebound among patients on highly active antiretroviral therapy (HAART) with previously undetectable levels of viraemia. Design: An observational cohort study of 2444 patients from the EuroSIDA study. Methods: Patients were followed from their first viral load under 400 copies/ml to the first of two consecutive viral loads above 400 copies/ml. Incidence rates were calculated using person-years of follow-up (PYFU), Cox proportional hazards models were used to determine factors related to rebound. Results: Of 2444 patients, 1031 experienced virological rebound (42.2%). The incidence of rebound decreased over time; from 33.5 in the first 6 months after initial suppression to 8.6 per 100 PYFU at 2 years after initial suppression (P < 0.0001). The rate of rebound was lower for treatment-naive compared with treatment-experienced patients. In multivariate models, patients who changed treatment were more likely to rebound, as were patients with higher viral loads on starting HAART. Treatment-naive patients were less likely to rebound. Among pretreated patients, those who were started on new nucleosides were less likely to rebound. Conclusion: The rate of virological rebound decreased over time, suggesting that the greatest risk of treatment failure is in the months after initial suppression. Treatment-naive patients were at a lower risk of rebound, but among drug-experienced patients, those who added new nucleosides had a lower risk of rebound, as were patients with a good immunological response. (C) 2003 Lippincott Williams & Wilkins.
引用
收藏
页码:1741 / 1751
页数:11
相关论文
共 37 条
[1]  
[Anonymous], 1992, MMWR Recomm Rep, V41, P1
[2]  
*BRIT HIV ASS, 2001, HIV MED, V2, P276
[3]   Sustained CD4+ T cell response after virologic failure of protease inhibitor-based regimens in patients with human immunodeficiency virus infection [J].
Deeks, SG ;
Barbour, JD ;
Martin, JN ;
Swanson, MS ;
Grant, RM .
JOURNAL OF INFECTIOUS DISEASES, 2000, 181 (03) :946-953
[4]   HIV RNA and CD4 cell count response to protease inhibitor therapy in an urban AIDS clinic: Response to both initial and salvage therapy [J].
Deeks, SG ;
Hecht, FM ;
Swanson, M ;
Elbeik, T ;
Loftus, R ;
Cohen, PT ;
Grant, RM .
AIDS, 1999, 13 (06) :F35-F43
[5]   Mechanisms of virologic failure in previously untreated HIV-infected patients from a trial of induction-maintenance therapy [J].
Descamps, D ;
Flandre, P ;
Calvez, V ;
Peytavin, G ;
Meiffredy, V ;
Collin, G ;
Delaugerre, C ;
Robert-Delmas, S ;
Bazin, B ;
Aboulker, JP ;
Pialoux, G ;
Raffi, F ;
Brun-Vézinet, F .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2000, 283 (02) :205-211
[6]   Drug-resistance genotyping in HIV-1 therapy: the VIRADAPT randomised controlled trial [J].
Durant, J ;
Clevenbergh, P ;
Halfon, P ;
Delgiudice, P ;
Porsin, S ;
Simonet, P ;
Montagne, N ;
Boucher, CAB ;
Schapiro, JM ;
Dellamonica, P .
LANCET, 1999, 353 (9171) :2195-2199
[7]   Virological treatment failure of protease inhibitor therapy in an unselected cohort of HIV-infected patients [J].
Fatkenheuer, G ;
Theisen, A ;
Rockstroh, J ;
Grabow, T ;
Wicke, C ;
Becker, K ;
Wieland, U ;
Pfister, H ;
Reiser, M ;
Hegener, P ;
Franzen, C ;
Schwenk, A ;
Salzberger, B .
AIDS, 1997, 11 (14) :F113-F116
[8]   Latent infection of CD4+ T cells provides a mechanism for lifelong persistence of HIV-1, even in patients on effective combination therapy [J].
Finzi, D ;
Blankson, J ;
Siliciano, JD ;
Margolick, JB ;
Chadwick, K ;
Pierson, T ;
Smith, K ;
Lisziewicz, J ;
Lori, F ;
Flexner, C ;
Quinn, TC ;
Chaisson, RE ;
Rosenberg, E ;
Walker, B ;
Gange, S ;
Gallant, J ;
Siliciano, RF .
NATURE MEDICINE, 1999, 5 (05) :512-517
[9]   Participation in research and access to experimental treatments by HIV-infected patients [J].
Gifford, AL ;
Cunningham, WE ;
Heslin, KC ;
Andersen, RM ;
Nakazono, T ;
Lieu, DK ;
Shapiro, MF ;
Bozzette, SA .
NEW ENGLAND JOURNAL OF MEDICINE, 2002, 346 (18) :1373-1382
[10]   Factors associated with clinical and virological failure in patients receiving a triple therapy including a protease inhibitor [J].
Grabar, S ;
Pradier, C ;
Le Corfec, E ;
Lancar, R ;
Allavena, C ;
Bentata, M ;
Berlureau, P ;
Dupont, C ;
Fabbro-Peray, P ;
Poizot-Martin, I ;
Costagliola, D .
AIDS, 2000, 14 (02) :141-149