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Updated: Jan 24, 2026

Gene Editing of Primary Rhesus Macaque B Cells
Published on: February 10, 2023
Cynomolgus macaque IL37 polymorphism and control of SIV infection
Takashi Shiina1, Shingo Suzuki1, Nicolas Congy-Jolivet2,3
1Department of Molecular Life Sciences, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Abstract:
The association between gene polymorphisms and plasma virus load at the set point (SP-PVL) was investigated in Mauritian macaques inoculated with SIV. Among 44 macaques inoculated with 50 AID50, six individuals were selected: three with SP-PVL among the highest and three with SP-PVL among the lowest. The exons of 390 candidate genes of these six animals were sequenced. Twelve non-synonymous single nucleotide polymorphisms (NS-SNPs) lying in nine genes potentially associated with PVL were genotyped in 23 animals. Three NS-SNPs with probabilities of association with PVL less than 0.05 were genotyped in a total of 44 animals. One NS-SNP lying in exon 1 of the IL37 gene displayed a significant association (p = 3.33 × 10-4) and a strong odds ratio (19.52). Multiple linear regression modeling revealed three significant predictors of SP-PVL, including the IL37 exon 1 NS-SNP (p = 0.0004) and the MHC Class IB haplotypes M2 (p = 0.0007) and M6 (p = 0.0013). These three factors in conjunction explained 48% of the PVL variance (p = 4.8 × 10-6). The potential role of IL37 in the control of SIV infection is discussed.
Insights
Genetic variations, specifically a non-synonymous single nucleotide polymorphism (NS-SNP) in the IL37 gene, are significantly associated with controlling simian immunodeficiency virus (SIV) plasma virus load in macaques.
Area of Science:
- Genetics and Immunology
- Virology
- Animal Models
Background:
- Simian immunodeficiency virus (SIV) infection in Mauritian macaques serves as a model for studying human immunodeficiency virus (HIV).
- Plasma virus load at set point (SP-PVL) is a critical determinant of disease progression in SIV-infected macaques.
Purpose of the Study:
- To investigate the association between gene polymorphisms and SP-PVL in Mauritian macaques.
- To identify genetic factors influencing viral load during chronic SIV infection.
Main Methods:
- Sequencing of candidate genes in macaques with high and low SP-PVL.
- Genotyping of non-synonymous single nucleotide polymorphisms (NS-SNPs) associated with PVL.
- Multiple linear regression modeling to identify predictors of SP-PVL.
Main Results:
- One NS-SNP in exon 1 of the IL37 gene showed a significant association with SP-PVL (p=3.33×10⁻⁴) and a high odds ratio (19.52).
- IL37 exon 1 NS-SNP, MHC Class IB haplotypes M2 and M6 were significant predictors of SP-PVL.
- These three factors explained 48% of the PVL variance (p=4.8×10⁻⁶).
Conclusions:
- The IL37 gene polymorphism is a significant predictor of SIV plasma virus load in Mauritian macaques.
- IL37 may play a role in controlling SIV infection.
- Combined genetic factors significantly influence viral load set point in SIV infection.
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