Buhusayen Feras A Majeed, Alashraaf Mohamed, Jadah Raafat Hamad Seroor H
General Surgery, Bahrain Defence Force Hospital, Royal Medical Services, Riffa, BHR.
General Surgery, King Hamad University Hospital, Royal Medical Services, Riffa, BHR.
Cureus. 2025 Apr 24;17(4):e82903. doi: 10.7759/cureus.82903. eCollection 2025 Apr.
The ARV1 gene produces a protein made up of 271 amino acids that helps transport fats across membranes within the cell's endoplasmic reticulum (ER), a key area involved in processing lipids. This protein is related to an enzyme called ACAT2, which is important for managing cholesterol and fat levels in the body. This protein features an N-terminal zinc-binding motif located in the cytosol, followed by multiple domains that span the ER membrane, and concludes with a C-terminus that terminates in the ER lumen. ARV1 deficiency clinically manifests as autosomal recessive developmental and epileptic encephalopathy 38 (DEE38) in humans. In this report, we share three pediatric cases presenting with early-onset epileptic encephalopathy and significant developmental delay. Whole-exome sequencing (WES) identified two pathogenic ARV1 variants: p.Cys61Tyr (missense) and p.Phe144Argfs5* (frameshift), both predicted to severely disrupt protein structure and function. These findings add to what we know about how mutations in the ARV1 gene can lead to developmental and epileptic encephalopathy (DEE38), and they strengthen our understanding of the gene's role in brain development. The children in our report also show how widely the symptoms of ARV1-related conditions can vary from case to case. Their experiences highlight just how important early genetic testing can be, especially for young patients with unexplained seizures and developmental challenges. Our report contributes to understanding the spectrum of complex neurological conditions. By sharing these cases, we're adding to the growing knowledge about ARV1-related encephalopathies and reinforcing why this gene deserves a place in targeted epilepsy genetic panels.
ARV1基因产生一种由271个氨基酸组成的蛋白质,该蛋白质有助于将脂肪转运穿过细胞内质网(ER)中的膜,内质网是参与脂质加工的关键区域。这种蛋白质与一种名为ACAT2的酶相关,ACAT2对控制体内胆固醇和脂肪水平很重要。这种蛋白质具有位于细胞质中的N端锌结合基序,随后是多个跨内质网膜的结构域,并以位于内质网腔中的C端结束。ARV1缺乏症在临床上表现为人类常染色体隐性发育性和癫痫性脑病38型(DEE38)。在本报告中,我们分享了三例表现为早发性癫痫性脑病和明显发育迟缓的儿科病例。全外显子组测序(WES)鉴定出两个致病性ARV1变体:p.Cys61Tyr(错义)和p.Phe144Argfs5*(移码),两者均预计会严重破坏蛋白质结构和功能。这些发现增加了我们对ARV1基因突变如何导致发育性和癫痫性脑病(DEE38)的了解,并加强了我们对该基因在大脑发育中作用的理解。我们报告中的儿童还展示了与ARV1相关病症的症状在不同病例之间的差异有多大。他们的经历凸显了早期基因检测有多重要,尤其是对于患有无法解释的癫痫发作和发育挑战的年轻患者。我们的报告有助于理解复杂神经系统疾病的范围。通过分享这些病例,我们增加了对与ARV1相关脑病的认识,并强化了为什么该基因应在靶向癫痫基因检测板中占有一席之地。