Association of SNP-SNP interactions of surfactant protein genes with severity of respiratory syncytial virus infection in children.

The severity of respiratory syncytial virus (RSV) may be linked to host genetic susceptibility. Surfactant protein (SP) genetic variants have been associated with RSV severity, but the impact of single-nucleotide polymorphism (SNP)-SNP interactions remains unexplored. Therefore, we used a novel statistical model to investigate the association of SNP-SNP interactions of genes with RSV severity in two- and three-interaction models.

Association of surfactant protein A2 with acute respiratory failure in children.

Background: Interactions among single nucleotide polymorphisms (SNPs) of surfactant protein (SP) are associated with acute respiratory failure (ARF) and its short-term outcome, pulmonary dysfunction at discharge (PDAD) in children. However, genetic association studies using individual SNPs have not been conducted before. We hypothesize that SP genetic variants are associated with pediatric ARF and its short-term complications by themselves.

Corrigendum: Single nucleotide polymorphisms interactions of the surfactant protein genes associated with respiratory distress syndrome susceptibility in preterm infants.

[This corrects the article DOI: 10.3389/fped.2021.

Hydrophilic But Not Hydrophobic Surfactant Protein Genetic Variants Are Associated With Severe Acute Respiratory Syncytial Virus Infection in Children.

Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infection-related hospitalization in the first year of life. Surfactant dysfunction is central to pathophysiologic mechanisms of various pulmonary diseases including RSV. We hypothesized that RSV severity is associated with single nucleotide polymorphisms (SNPs) of surfactant proteins (SPs).

The Lung Alveolar Cell (LAC) miRNome and Gene Expression Profile of the SP-A-KO Mice After Infection With and Without Rescue With Human Surfactant Protein-A2 (1A).

Human surfactant protein (SP)-A1 and SP-A2 exhibit differential qualitative and quantitative effects on the alveolar macrophage (AM), including a differential impact on the AM miRNome. Moreover, SP-A rescue (treatment) of SP-A-knockout (KO) infected mice impoves survival. Here, we studied for the first time the role of exogenous SP-A protein treatment on the regulation of lung alveolar cell (LAC) miRNome, the miRNA-RNA targets, and gene expression of SP-A-KO infected mice of both sexes.