Role of HLA-B Leader Peptides and HLA-E Genetic Variants in HIV Infection

Abstract

Objective: This study assessed whether human leukocyte antigen (HLA)-B signal peptide dimorphism at position −21 (HLA-B-21) Methionine/Threonine (M/T) and HLA-E polymorphisms are associated with the level of viremia in human immunodeficiency virus (HIV)-positive individuals from the Turkish population. Materials and Methods: The study cohort comprised 130 HIV–positive patients and 102 healthy controls. HLA typing was achieved through a next-generation sequencing (NGS)–based approach, and HLA-E alleles were determined by Sanger sequencing. HIV-1 level of viremia was measured using the COBAS Ampliprep/TaqMan system. Statistical evaluation included chi-square analysis, nonparametric techniques, and logistic regression modeling. Results: HLA-E*01:01 and the homozygous E*01:01 genotype were observed significantly more frequently in HIV–positive patients than in controls. No significant relationship was found between HLA-E alleles and viral load. The HLA-B*51:01 allele was significantly more frequent in patients with a higher viral load, whereas HLA-B*44:02 showed a similar trend without reaching statistical significance. In addition, the HLA-B-21 T/T genotype was significantly associated with higher viral load levels. Conclusion: Our findings indicate that the HLA-B-21 signal peptide polymorphism may play a role in modulating HIV replication, whereas HLA-E polymorphisms alone appear to have a limited impact. This study provides novel immunogenetic data from the Turkish population and highlights the potential of HLA-B-21 polymorphism as a genetic marker influencing HIV disease progression.

Keywords

• HIV
• HLA-B signal peptide
• HLA-E polymorphism
• viral loads.

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