Clinical and Diagnostic Laboratory Immunology, July 1998, p. 463-466, Vol. 5, No. 4
1071-412X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Divisions of Clinical Virology (F 68),1 Clinical and Oral Bacteriology (F 88),3 and Infectious Diseases,4 Karolinska Institutet, Huddinge University Hospital, S-141 86 Huddinge, Sweden, and Department of Infectious and Tropical Diseases, University of Rome "La Sapienza," Rome, Italy2
Received 24 November 1997/Returned for modification 15 January 1998/Accepted 19 March 1998
The correlation among the presence of a 32-bp deletion in the
CC-chemokine receptor 5 (CCR5) gene, disease progression,
and human immunodeficiency virus type 1 (HIV-1)-specific immune
responses was analyzed for a cohort of 79 Caucasian HIV-1-infected
patients. The CCR5 genotype (CCR5/CCR5 = wild type/wild type or
32CCR5/CCR5 = 32-bp
deletion/wild type) in peripheral blood mononuclear cells was
determined by PCR, followed by sequencing of both wild-type and
32CCR5 gene fragments. HIV-1-specific humoral responses
to gp41 and V3MN peptides were determined by enzyme
immunoassays. The prevalence of the
32CCR5 allele was
lower among 37 patients with rapid progression (progression to AIDS or
to a CD4 cell count of <200 × 106/liter in less than
9 years; P < 0.01) compared to that for 42 patients
with slow progression (no AIDS and CD4 cell count of >200 × 106/liter after at least 9 years from infection) or to that
for 25 non-HIV-1-infected Swedish blood donors (P < 0.05). No differences were observed in the wild-type CCR5
sequences between the different groups of patients. For three analyzed
patients, the 32-bp
32CCR5 gene deletions were
identical. The antibody titers against gp41 and a V3MN
peptide in patients with the
32CCR5/CCR5 genotype were
not significantly different from those in pair-matched
CCR5/CCR5 controls. However, in 13 analyzed patients, a
stronger serum neutralizing activity was associated with the
32CCR5/CCR5 genotype. Thus, a CCR5/CCR5
genotype correlates with a shortened AIDS-free HIV-1 infection period
and possibly with a worse neutralizing activity, without an evident
influence on the antibody response to two major antigenic regions of
HIV-1 envelope.
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