Investigation of susceptibility genes for chickenpox disease across multiple continents.

Chickenpox (varicella) is caused by infection with the varicella-zoster virus (VZV), a neurotropic alpha herpes virus with a double-stranded DNA genome. Chickenpox can cause life-threatening complications, including subsequent bacterial infections, central nervous system symptoms, and even death without any risk factors. Few studies have been reported to investigate genetic susceptibility implicated in chickenpox. Herein, our study identified global genetic variants that potentially contributed to chickenpox susceptibility by utilizing the established bioinformatic-based approach. We integrated several databases, such as genome-wide association studies (GWAS) catalog, GTEx portal, HaploReg version 4.1, and Ensembl databases analyses to investigate susceptibility genes associated with chickenpox. Notably, increased expression of HLA-S, HCG4P5, and ABHD16A genes underlie enhanced chickenpox susceptibility in the European, American, and African populations. As compared to the Asian population, Europeans, Americans, and Africans have higher allele frequencies of the extant variants rs9266089, rs10947050, and rs79501286 from the susceptibility genes. Our study suggested that these susceptibility genes and associated genetic variants might play a critical role in chickenpox progression based on host genetics with clinical implications.

Identification of Hub Genes and Potential Biomarkers for Childhood Asthma by Utilizing an Established Bioinformatic Analysis Approach.

Childhood asthma represents a heterogeneous disease resulting from the interaction between genetic factors and environmental exposures. Currently, finding reliable biomarkers is necessary for the clinical management of childhood asthma. However, only a few biomarkers are being used in clinical practice in the pediatric population. In the long run, new biomarkers for asthma in children are required and would help direct therapy approaches. This study aims to identify potential childhood asthma biomarkers using a genetic-driven biomarkers approach. Herein, childhood asthma-associated Single Nucleotide Polymorphisms (SNPs) were utilized from the GWAS database to drive and facilitate the biomarker of childhood asthma. We uncovered 466 childhood asthma-associated loci by extending to proximal SNPs based on r2 > 0.8 in Asian populations and utilizing HaploReg version 4.1 to determine 393 childhood asthma risk genes. Next, the functional roles of these genes were subsequently investigated using Gene Ontology (GO) term enrichment analysis, a Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and a protein−protein interaction (PPI) network. MCODE and CytoHubba are two Cytoscape plugins utilized to find biomarker genes from functional networks created using childhood asthma risk genes. Intriguingly, 10 hub genes (IL6, IL4, IL2, IL13, PTPRC, IL5, IL33, TBX21, IL2RA, and STAT6) were successfully identified and may have been identified to play a potential role in the pathogenesis of childhood asthma. Among 10 hub genes, we strongly suggest IL6 and IL4 as prospective childhood asthma biomarkers since both of these biomarkers achieved a high systemic score in Cytohubba's MCC algorithm. In summary, this study offers a valuable genetic-driven biomarker approach to facilitate the potential biomarkers for asthma in children.