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LILRA3 deletion is a genetic risk factor of HIV infection. | LitMetric

LILRA3 deletion is a genetic risk factor of HIV infection.

AIDS

aClinic for Immunology and Rheumatology, Hannover Medical School (MHH), Hannover bDepartment of Infectious Diseases cDepartment of Infectious Diseases Epidemiology, Robert Koch-Institute, Berlin dAESKU Diagnostics, Wendelsheim eGerman Center for Infection Research (DZIF), Partner-site Hannover-Braunschweig, Hannover, Germany.

Published: January 2017

AI Article Synopsis

  • This study investigates how the deletion of the LILRA3 gene affects the transmission and progression of HIV infection.
  • Researchers found that individuals with the homozygous deletion of LILRA3 were more likely to be HIV-positive and experienced faster disease progression, with a notable difference in short-term progressors compared to those with other genotypes.
  • The study concluded that having this gene deletion increases susceptibility to HIV and leads to worsened outcomes for affected individuals.

Article Abstract

Objective: The aim of this study is to analyse the influence of LILRA3 and the genetic leukocyte immunoglobulin-like receptor 3 (LILRA3) deletion on transmission and clinical course of HIV infection.

Design: Case and control study.

Methods: LILRA3 genotypes were determined by PCR. HIV patients were categorized into short-term progressors, normal progressors and long-term nonprogressors according to the clinical course. Functional studies were performed using real-time PCR, intracellular flow cytometry and ELISA.

Results: The prevalence of the homozygous LILRA3 deletion was higher in HIV-positive individuals (n = 439) than in controls (n = 651) (P = 0.02). The disease progression was faster in homozygously deleted patients with more short-term progressors than in heterozygous (P = 0.03) and homozygously positive (P = 0.002) individuals. These results have been confirmed in a seroconverter cohort (n = 288). The frequency of the homozygous deletion in the confirmation cohort was higher than in controls (P = 0.04). Combining both cohorts, the proportion of homozygously LILRA3-deleted individuals was 6.2% in HIV-infected patients (n = 727) vs. 3.2% in controls (P = 0.01). Functional analysis revealed an upregulation of the LILRA3 gene in real-time PCR in treated patients when compared with untreated patients (P = 0.007) and controls (P = 0.02) resulting in a higher LILRA3 expression in CD4 (P = 0.008) and CD14 (P = 0.02) cells of untreated patients in intracellular flow cytometry. LILRA 3 concentrations in the sera were similar between the groups, in untreated patients a correlation between viral load and LILRA3 concentration was found.

Conclusion: The homozygous LILRA3 deletion is associated with a higher susceptibility for HIV disease and with a faster disease progression.

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Source
http://dx.doi.org/10.1097/QAD.0000000000001304DOI Listing

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