Related Experiment Video
Updated: Jun 24, 2026

14:23
A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
Published on: August 31, 2014
Extended IL10 haplotypes and their association with HIV progression to AIDS
T K Oleksyk1, S Shrestha, A L Truelove
1Laboratory of Genomic Diversity, and Basic Research Program, Science Applications International Corporation-Frederick, National Cancer Institute at Frederick, Frederick, MD 21702, USA.
Genes and Immunity
|March 20, 2009
Summary
Interleukin-10 (IL-10) gene variations influence disease progression. Certain IL-10 haplotypes, like ATA-inclusive, are linked to faster AIDS progression in European Americans, highlighting genetic roles in immune response.
Area of Science:
- Immunogenetics
- Human evolutionary genetics
Background:
- Interleukin-10 (IL-10) is a cytokine with dual immune functions, crucial in infections and autoimmunity.
- Genetic polymorphisms in the IL10 gene may reflect evolutionary adaptations to pathogens and autoimmune diseases.
Purpose of the Study:
- To investigate the evolutionary heterogeneity of human IL10 gene polymorphisms.
- To examine the association between IL10 haplotypes and HIV progression.
Main Methods:
- Genotyped 21 single nucleotide polymorphisms (SNPs) in the human IL10 gene.
- Compared human IL10 variation with sequences from other mammalian species.
- Analyzed haplotype associations with HIV progression using haplotype trend regression.
Main Results:
- Identified three main human IL10 haplotype groups: high-producing GCC, intermediate ACC, and low-producing ATA.
- ATA-inclusive haplotypes, associated with lower IL-10 production, showed a trend towards faster AIDS progression in European Americans.
- Haplotype heterogeneity suggests evolutionary balancing selection related to pathogen and autoimmune pressures.
Conclusions:
- IL10 gene polymorphisms, particularly the ATA-inclusive haplotype, are associated with accelerated HIV/AIDS progression.
- These findings support the hypothesis that IL10 genetic variations represent adaptive responses to historical disease agents.

