Talebi Taravat, Biglari Alireza, Shahroeei Mohammad, Changi-Ashtiani Majid, Dinmohammadi Hossein, Navabi Shadi Sadat, Parvaneh Nima, Bossuyt Xavier, Shahani Tina, Rokni-Zadeh Hassan
Department of Genetics and Molecular Medicine, School of Medicine, Zanjan University of Medical Sciences (ZUMS), Zanjan, Iran.
Clinical and Diagnostic Immunology, Department of Microbiology and Immunology, KU Leuven, Leuven, Belgium AND Specialised Immunology Laboratory of Dr. Shahrooei, Ahvaz, Iran.
Iran J Allergy Asthma Immunol. 2020 Feb 1;19(1):94-101. doi: 10.18502/ijaai.v19i1.2422.
Severe combined immunodeficiency (SCID) comprises a heterogeneous group of genetic disorders caused by early defects in the development and function of T cells. Other lymphocyte lineages (B and/or natural killer cells) are variably affected. With a worldwide frequency of approximately 1:50,000 live births, SCID may result from diverse mutations in over 16 genes. Whole-exome sequencing (WES) provides an opportunity for parallel screening of all those genes. This approach is also useful for genetic diagnosis in parents whose infant expired before genetic testing. Here, we describe a heterozygous novel non-frameshift deletion (c.587_598del p.196_199del) in the adenosine deaminase (ADA) gene identified by WES in healthy parents of an expired child with SCID. The mutation was subsequently confirmed to be homozygous in the deceased baby whose left-over blood sample volume was insufficient for direct WES analysis. In conclusion, we here describe a novel mutation in ADA, a well-known SCID gene.
重症联合免疫缺陷病(SCID)是一组由T细胞发育和功能早期缺陷引起的遗传性疾病,具有异质性。其他淋巴细胞谱系(B细胞和/或自然杀伤细胞)也受到不同程度的影响。SCID在全球活产婴儿中的发病率约为1:50000,可能由16种以上基因的不同突变引起。全外显子测序(WES)为平行筛查所有这些基因提供了机会。这种方法对于婴儿在基因检测前死亡的父母的基因诊断也很有用。在此,我们描述了在一名患有SCID的已故儿童的健康父母中,通过WES在腺苷脱氨酶(ADA)基因中鉴定出的一种杂合性新型非移码缺失(c.587_598del p.196_199del)。随后在已故婴儿中证实该突变是纯合的,但其剩余血样量不足以进行直接WES分析。总之,我们在此描述了一个在著名的SCID基因ADA中的新型突变。