Therapeutic response of HIV-1 subtype C in African patients coinfected with either Mycobacterium tuberculosis or human herpesvirus-8

被引:24
作者
Cassol, E [1 ]
Page, T
Mosam, A
Friedland, G
Jack, C
Lalloo, U
Kopetka, J
Patterson, B
Esterhuizen, T
Coovadia, HM
机构
[1] Univ KwaZulu Natal, Nelson R Mandela Sch Med, Doris Duke Med Res Inst,Africa Ctr Hlth & Populat, HIV1 Mol Virol & Bioinformat Unit, Durban, South Africa
[2] Univ KwaZulu Natal, Doris Duke Med Res Inst, Ctr HIV AIDS Networking, Durban, South Africa
[3] Univ KwaZulu Natal, Nelson R Mandela Sch Med, Dept Dermatol, Durban, South Africa
[4] Univ KwaZulu Natal, Nelson R Mandela Sch Med, Dept Med, Durban, South Africa
[5] Univ KwaZulu Natal, Fac Hlth Sci, Durban, South Africa
[6] Yale Univ, Sch Med, New Haven, CT USA
[7] Invir Inc, Frankfort, MI USA
[8] Stanford Univ, Sch Med, Dept Clin Virol, Palo Alto, CA 94304 USA
基金
英国惠康基金;
关键词
D O I
10.1086/427337
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background. A potential confounding factor in the treatment of human immunodeficiency virus (HIV) infection in Africa is the frequent occurrence of opportunistic infections (OIs). OI-induced immune activation can interfere with HIV-1 clearance by increasing viral replication and target cell availability. Study design. Treatment outcomes for patients dually infected with HIV-1 and Mycobacterium tuberculosis or HIV-1 and human herpesvirus (HHV)-8 were assessed by measuring changes in viral load and CD4(+) cell counts and by determining the time taken to reach undetectable HIV-1 RNA levels, assessed by means of Kaplan-Meier survival analysis. Patients with HIV-1 and Kaposi sarcoma (KS) received generic nevirapine, stavudine, and lamivudine (3TC); patients with HIV-1 and tuberculosis (TB) received standard commercial didanosine, 3TC, and efavirenz. Results. Both cohorts exhibited a rapid, near-exponential phase I decline in viral load. Patients with TB and late-stage KS had the steepest decay kinetics. These same patients had the greatest initial increase in CD4(+) cell counts. Phase II clearance was slower and more variable. The proportions of patients reaching undetectable plasma HIV-1 levels at days 7, 14, 28, 60, and 90 were, respectively, 15.8%, 30.0%, 52.6%, 78.9%, and 93.8% (Pearson's chi(2) = 50.5; P<.001) for patients with TB and 0.0%, 5.0%, 22.2%, 64.7%, and 80.0% (Pearson's χ(2) = 63.6; P < .001) for patients with KS. Conclusions. Nucleoside reverse-transcriptase inhibitor/nonnucleoside reverse-transcriptase inhibitor-based treatment regimens are highly effective in clearing rapidly replicating (phase I) virus in African patients dually infected with HIV-1 and either TB or KS.
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收藏
页码:324 / 332
页数:9
相关论文
共 61 条
[1]   Prevalence of genotypic and phenotypic HIV-1 drug-resistant strains among patients who have rebound in viral load while receiving antiretroviral therapy in the UNAIDS-Drug Access Initiative in Abidjan, Cote d'Ivoire [J].
Adjé-Touré, C ;
Celestin, B ;
Hanson, D ;
Roels, TH ;
Hertogs, K ;
Larder, B ;
Diomande, F ;
Peeters, M ;
Eholié, S ;
Lackritz, E ;
Chorba, T ;
Nkengasong, JN .
AIDS, 2003, 17 :S23-S29
[2]  
Aquaro S, 1998, Clin Ter, V149, P37
[3]   Inhibition of replication of HIV in primary monocyte/macrophages by different antiviral drugs and comparative efficacy in lymphocytes [J].
Aquaro, S ;
Perno, CF ;
Balestra, E ;
Balzarini, J ;
Cenci, A ;
Francesconi, M ;
Panti, S ;
Serra, F ;
Villani, N ;
Calio, R .
JOURNAL OF LEUKOCYTE BIOLOGY, 1997, 62 (01) :138-143
[4]   Biphasic decay of latently infected CD4+ T cells in acute human immunodeficiency virus type 1 infection [J].
Blankson, JN ;
Finzi, D ;
Pierson, TC ;
Sabundayo, BP ;
Chadwick, K ;
Margolick, JB ;
Quinn, TC ;
Siliciano, RF .
JOURNAL OF INFECTIOUS DISEASES, 2000, 182 (06) :1636-1642
[5]  
CASSOL E, 2004, MEDGENMED, V6
[6]   The contribution of monocyte infection and trafficking to viral persistence, and maintenance of the viral reservoir in HIV infection [J].
Crowe, S ;
Zhu, TF ;
Muller, WA .
JOURNAL OF LEUKOCYTE BIOLOGY, 2003, 74 (05) :635-641
[7]  
Crowe SM, 2000, J LEUKOCYTE BIOL, V68, P345
[8]  
*DEP HLTH DIR HLTH, 2001, 7 NAT HIV SURV WOM A
[9]  
DEWIT S, 2003, ANTIVIR THER S, V8, P5190
[10]  
DOYLE PR, 1992, 23 U WITW DEP COMM H