Pontifícia Universidade Católica do Paraná, Curitiba, PR, Brazil.
Fundação de Medicina Tropical Dr. Heitor Vieira Dourado, Manaus, AM, Brazil.
An Bras Dermatol. 2022 May-Jun;97(3):298-306. doi: 10.1016/j.abd.2021.08.004. Epub 2022 Mar 21.
Leishmaniasis is caused by an intracellular protozoan of the Leishmania genus. Mannose-binding lectin (MBL) is a serum complement protein and recognizes lipoprotein antigens in protozoa and the bacterial plasma membrane. Nucleotide variants in the promoter region and exon 1 of the MBL gene can influence its expression or change its molecular structure.
To evaluate, through a systematic review, case-control studies of the genetic association of variants in the MBL2 gene and the risk of developing leishmaniasis.
This review carried out a search in PubMed, Science Direct, Cochrane Library, Scopus and Lilacs databases for case-control publications with six polymorphisms in the mannose-binding Lectin gene. The following strategy was used: P = Patients at risk of leishmaniasis; I = Presence of polymorphisms; C = Absence of polymorphisms; O = Occurrence of leishmaniasis. Four case/control studies consisting of 791 patients with leishmaniasis and 967 healthy subjects (Control) are included in this meta-analysis. The association of variants in the mannose-binding Lectin gene and leishmaniasis under the allelic genetic model, -550 (Hvs. L), -221 (X vs. Y), +4 (Q vs. P), CD52 (A vs. D), CD54 (A vs. B), CD57 (A vs. C) and A/O genotype (A vs. O) was evaluated. International Prospective Register of Systematic Reviews (PROSPERO): CRD42020201755.
The meta-analysis results for any allelic genetic model showed no significant association for the variants within the promoter, the untranslated region, and exon 1, as well as for the wild-type A allele and mutant allele O with leishmaniasis.
Caution should be exercised when interpreting these results, as they are based on a few studies, which show divergent results when analyzed separately.
This meta-analysis showed a non-significant association between the rs11003125, rs7096206, rs7095891, rs5030737, rs1800450, and rs1800451 polymorphisms of the Mannose-binding Lectin gene and leishmaniasis in any allelic and heterogeneous evaluation.
利什曼病是由利什曼原虫属的细胞内原生动物引起的。甘露糖结合凝集素(MBL)是一种血清补体蛋白,可识别原生动物和细菌质膜中的脂蛋白抗原。MBL 基因启动子区域和外显子 1 中的核苷酸变异可影响其表达或改变其分子结构。
通过系统评价评估 MBL2 基因变异与利什曼病发病风险的遗传相关性的病例对照研究。
本研究在 PubMed、Science Direct、Cochrane Library、Scopus 和 Lilacs 数据库中进行了病例对照文献检索,共检索到 6 种甘露糖结合凝集素基因多态性的病例对照研究。采用以下策略:P=患利什曼病的患者;I=存在多态性;C=不存在多态性;O=发生利什曼病。本 meta 分析纳入了 4 项病例对照研究,共纳入 791 例利什曼病患者和 967 例健康对照者(对照组)。评估了甘露糖结合凝集素基因变异与等位基因遗传模型下的利什曼病的相关性,包括 -550(Hvs.L)、-221(Xvs.Y)、+4(Qvs.P)、CD52(Avs.D)、CD54(Avs.B)、CD57(Avs.C)和 A/O 基因型(Avs.O)。国际前瞻性系统评价注册中心(PROSPERO):CRD42020201755。
任何等位基因遗传模型的荟萃分析结果均显示,启动子、非翻译区和外显子 1 中的变异以及野生型 A 等位基因和突变型 O 等位基因与利什曼病均无显著相关性。
由于这些结果基于少数研究,因此在解释这些结果时应谨慎,这些研究单独分析时显示出不同的结果。
本荟萃分析显示,在任何等位基因和异质性评价中,甘露糖结合凝集素基因的 rs11003125、rs7096206、rs7095891、rs5030737、rs1800450 和 rs1800451 多态性与利什曼病无显著相关性。