CCR5 Δ32 Deletion and Reduced Risk of Toxoplasmosis in Persons Infected with Human Immunodeficiency Virus Type 1
Author(s) -
Laurence Meyer,
Magda Magierowska,
JeanBaptiste Hubert,
MarieJeanne Mayaux,
Micheline Misrahi,
Jérôme Le Chenadec,
Patrice Debré,
Christine Rouzioux,
JeanFrançois Delfraissy,
Ioannis Théodorou
Publication year - 1999
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/314933
Subject(s) - toxoplasmosis , immunology , cytomegalovirus , medicine , opportunistic infection , lymphoma , virology , immunodeficiency , virus , viral disease , herpesviridae , immune system
This study attempted to determine whether the CCR5 Delta32 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 Delta32 deletion could delay progression to certain opportunistic infections such as toxoplasmosis.
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