Candidate gene variants of the immune system and sudden infant death syndrome

Abstract

Our study did not replicate published associations of IL10 variants with SIDS. However, the evidence for two independent MBL2 variants in the combined analysis of two large series seems consistent with the hypothesis that infection may play a role in SIDS pathogenesis.

Identification of IL6 as a susceptibility gene for major depressive disorder

“…As MDD etiology is known to be linked to inflammation in at least some cases and immune response has been proven to be genetically influenced 19 , it is speculated that genetic factors in immune dysfunction may be involved in the pathophysiology of MDD 20 . IL6, a key proinflammatory cytokine 21 , has been reported in the development of MDD in prior literature.…”

Comment on Fard et al.’s Candidate gene variants of the immune system and sudden infant death syndrome

“…Fard et al [1] have done an excellent and thorough genetic investigation of 40 single nucleotide polymorphisms (SNPs) from 15 candidate genes for association with the sudden infant death syndrome (SIDS) and conclude that their results are consistent with the hypothesis that infection may play a role in SIDS pathogenesis. The team investigated SIDS cases collected at Hannover Medical School that included 267 Caucasian infants from Germany (163 males and 104 females).…”

“…Fard et al [1] did mention that Moon et al [10] reported a similar 60 % of male SIDS in their study with an understatement that "gender seems to be an important risk factor." But they did not reach the same conclusion as Naeye et al [4] who stated: "The general disadvantage of male infants has long been recognized.…”

Noncardiac genetic predisposition in sudden infant death syndrome

“…Our current study now examines the potential contribution of "non-cardiac" genes in the pathogenesis of SIDS using a similar approach to examine 61 published non-cardiac genes previously implicated in SIDS 8,[17][18][19][20][21] . The majority had been identified as potential "SIDS-susceptibility" genes following both common and rare variant association studies, typically involving promoter region variants.…”

“…8 Based on our own literature search of articles from 2014 to 2018, 6 additional SIDS-susceptibility genes were included for a total list of 61 non-cardiac, candidate genes (see Online Supplement eTable 1). [17][18][19][20][21] Following exome sequencing, single nucleotide variants (SNVs) and insertion/deletions (INDELs) were filtered to identify variants which followed either a dominant or recessive inheritance pattern using Ingenuity Variant Software (Qiagen, Redwood City, CA). All variants within the 61 non-cardiac SIDS-susceptibility genes were first filtered for a call quality score ≥ 20 and a read depth ≥ 10.…”