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<p>The <i>CCR5Δ32</i> polymorphism is a 32-base pair deletion in the <i>CCR5</i> gene that has been associated with slower HIV disease progression. However, its role in immune reconstitution during antiretroviral therapy (ART) remains unclear. We analyzed 236 virologically suppressed people living with HIV (PLHIV) after 24 months of ART, comprising 217 individuals homozygous for the wild-type <i>CCR5</i> allele and 19 heterozygous carriers of <i>CCR5Δ32</i>. Heterozygotes exhibited a significantly higher frequency of central memory CD4+ T cells compared with wild-type homozygotes (40.33 ± 8.79 vs. 32.71 ± 7.06; <i>p</i> = 0.0196), along with a tendency toward increased effector CD4+ T cells (5.100 [1.818–7.588] vs. 2.260 [1.485–3.503]; <i>p</i> = 0.0459). In contrast, longitudinal follow-up revealed that wild-type homozygotes achieved higher absolute CD4+ T cell counts at both 18 and 24 months of ART (<i>p</i> &lt; 0.05). These results suggest that <i>CCR5Δ32</i> contributes to qualitative preservation of CD4+ T cell subsets while limiting quantitative immune reconstitution, thereby providing novel insights into the long-term immunological impact of this polymorphism in virologically suppressed PLHIV.</p>

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CCR5Δ32 polymorphism is associated with increased central memory CD4+ T cells in virologically suppressed people living with HIV on antiretroviral therapy

  • 期刊论文

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  • 发表日期：

    2026年4月6日

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  • Henrique Fernando Lopes-Araujo,
  • Wlisses Henrique Veloso Carvalho-Silva,
  • José Leandro Andrade-Santos,
  • Maria Carolina Santos Guedes,
  • Fabrício Oliveira Souto,
  • Luiz Cláudio Arraes De Alencar,
  • Isadora Bandeira De Luna Paes Barreto Brennand,
  • Thayana Karinne Oliveira Monteiro,
  • Kleyverson Feliciano-Santos,
  • José Artur Bogo Chies,
  • Rafael Lima Guimarães

摘要

The CCR5Δ32 polymorphism is a 32-base pair deletion in the CCR5 gene that has been associated with slower HIV disease progression. However, its role in immune reconstitution during antiretroviral therapy (ART) remains unclear. We analyzed 236 virologically suppressed people living with HIV (PLHIV) after 24 months of ART, comprising 217 individuals homozygous for the wild-type CCR5 allele and 19 heterozygous carriers of CCR5Δ32. Heterozygotes exhibited a significantly higher frequency of central memory CD4+ T cells compared with wild-type homozygotes (40.33 ± 8.79 vs. 32.71 ± 7.06; p = 0.0196), along with a tendency toward increased effector CD4+ T cells (5.100 [1.818–7.588] vs. 2.260 [1.485–3.503]; p = 0.0459). In contrast, longitudinal follow-up revealed that wild-type homozygotes achieved higher absolute CD4+ T cell counts at both 18 and 24 months of ART (p < 0.05). These results suggest that CCR5Δ32 contributes to qualitative preservation of CD4+ T cell subsets while limiting quantitative immune reconstitution, thereby providing novel insights into the long-term immunological impact of this polymorphism in virologically suppressed PLHIV.