CCR5 Δ32 deletion and reduced risk of toxoplasmosis in persons infected with human immunodeficiency virus type 1

被引:23
作者
Meyer, L
Magierowska, M
Hubert, JB
Mayaux, MJ
Misrahi, M
Le Chenadec, J
Debre, P
Rouzioux, C
Delfraissy, JF
Theodorou, I
机构
[1] Hop Kremlin Bicetre, INSERM, U292, Serv Epidemiol, F-94276 Le Kremlin Bicetre, France
[2] Hop Kremlin Bicetre, Dept Med, F-94276 Le Kremlin Bicetre, France
[3] Hop Kremlin Bicetre, Lab Hormonol & Biol Mol, F-94276 Le Kremlin Bicetre, France
[4] Hop La Pitie Salpetriere, CNRS, URA 625, Lab Immunol Cellulaire & Tissulaire, Paris, France
[5] Hop Necker Enfants Malad, Dept Virol, Paris, France
关键词
D O I
10.1086/314933
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
This study attempted to determine whether the CCR5 Delta 32 deletion affected progression to certain first AIDS-defining illnesses in human immunodeficiency virus type 1-infected patients enrolled in the French SEROCO/HEMOCO/SEROGEST cohorts. Toxoplasmosis onset as a first AIDS-defining illness was significantly delayed in 253 heterozygous patients, compared with 1404 wild type patients. The relative risk of toxoplasmosis associated with heterozygosity was 0.39 (95% confidence interval, 0.16-0.96) after adjustment for age, CD4 cell count, and primary specific prophylaxis. A nonsignificant protective trend was observed with regard to the onset of mycobacterial, cytomegalovirus, and herpesvirus diseases, but these events were less frequent than toxoplasmosis. Progression to other conditions (e.g., wasting, non-Hodgkin's lymphoma, Kaposi's sarcoma) was similar in the 2 groups as was the frequency of toxoplasmosis as a subsequent AIDS-defining illness. As chemokines are involved in numerous infectious processes, the Delta 32 deletion could delay progression to certain opportunistic infections such as toxoplasmosis.
引用
收藏
页码:920 / 924
页数:5
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