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Sci Rep. 2019 May 28;9(1):7981. doi: 10.1038/s41598-019-44235-x.

Cynomolgus macaque IL37 polymorphism and control of SIV infection.

Author information

1
Department of Molecular Life Sciences, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
2
Laboratoire d'immunogénétique moléculaire (LIMT, EA 3034, Faculté de médecine Purpan, Université Toulouse 3, Paul Sabatier, UPS), Toulouse, France.
3
Laboratoire d'immunologie, CHU de Toulouse, Institut Fédératif de Biologie, hôpital Purpan, 330 Avenue de Grande Bretagne, TSA40031, 31059, Toulouse, cedex 9, France.
4
Inserm U1173, Simone Veil School of Health Sciences, University of Versailles Saint-Quentin-en-Yvelines, Montigny-le-Bretonneux, France.
5
Genetics Division, Ambroise Paré Hospital (AP-HP), Boulogne-Billancourt, France.
6
CEA - Université Paris-Sud 11 - INSERM U1184, Immunology of Viral Infections and Autoimmune Diseases, IDMIT Department, IBFJ, 92265, Fontenay-aux-Roses, France.
7
U1135, CIMI, INSERM, Paris, France, Sorbonne Universités, UPMC Université Paris 06, Paris, France, Département d'Immunologie, Hôpital Pitié-Salpêtrière, AP-HP, Paris, France.
8
Assistance Publique - Hôpitaux de Paris, Service de Médecine Interne et Immunologie Clinique, Groupe Hospitalier Universitaire Paris Sud, Hôpital Bicêtre, Le Kremlin-Bicêtre, France, Université Paris Sud, Le Kremlin Bicêtre, France.
9
Center for Immunology and Infectious Diseases, INSERM UMR S 1135, Pierre et Marie Curie University, Paris, France.
10
Laboratoire d'immunogénétique moléculaire (LIMT, EA 3034, Faculté de médecine Purpan, Université Toulouse 3, Paul Sabatier, UPS), Toulouse, France. blancher.antoine@neuf.fr.
11
Laboratoire d'immunologie, CHU de Toulouse, Institut Fédératif de Biologie, hôpital Purpan, 330 Avenue de Grande Bretagne, TSA40031, 31059, Toulouse, cedex 9, France. blancher.antoine@neuf.fr.
12
Centre de Physiopathologie Toulouse-Purpan (CPTP), Université de Toulouse, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (Inserm), Université Paul Sabatier (UPS), Toulouse, France. blancher.antoine@neuf.fr.

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.

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