Frequency of a mutated CCR-5 allele (Delta 32) among Italian healthy donors and individuals at risk of parenteral HIV infection

Citation
R. Zamarchi et al., Frequency of a mutated CCR-5 allele (Delta 32) among Italian healthy donors and individuals at risk of parenteral HIV infection, AIDS RES H, 15(4), 1999, pp. 337-344
Citations number
37
Categorie Soggetti
Immunology
Journal title
AIDS RESEARCH AND HUMAN RETROVIRUSES
ISSN journal
08892229 → ACNP
Volume
15
Issue
4
Year of publication
1999
Pages
337 - 344
Database
ISI
SICI code
0889-2229(19990301)15:4<337:FOAMCA>2.0.ZU;2-4
Abstract
The aim of this study was to assess the frequency of a truncated allele of the CCR-5 gene (Delta 32) in Italy, and address its possible role in parent eral HIV transmission, as well as its influence in HIV-associated disease p rogression. In 371 unrelated seronegative healthy blood donors the Delta 32 allele frequency was 0.047; this figure was significantly different from t hose reported in northern America and northern Europe populations. However, Delta 32 allele frequency in healthy individuals did not differ significan tly from that found in 54 seronegative drug users (0.065), 98 seronegative hemophiliacs (0.051), and 81 seropositive hemophiliacs (0.049). Although in seropositive hemophiliacs the wt/Delta 32 heterozygous genotype was associ ated with a trend to a slower decline in CD4(+) cell counts, its presence d id not seem to influence disease progression, as comparable Delta 32 allele frequency frequencies were found among progressing (0.042) and nonprogress ing (0.111) patients. These data do not seem to support a protective role o f the Delta 32 allele in preventing HIV infection through the parenteral ro ute, or in influencing the natural history of the disease in this particula r risk category, although the Delta 32 heterozygous state was associated wi th lower plasma viremia levels, On the other hand, the finding of non-syncy tium-inducing HIV strains in the majority of Delta 32 heterozygous seroposi tive patients suggests that its presence could not be a major factor in dri ving a switch toward more cytopathic, T-tropic HIV strains through selectiv e pressure in coreceptor usage.