Aim Respiratory Syncytial Virus (RSV) remains among the prevalent aetiologies of childhood lower respiratory tract infections with clinical entities that may vary between children possibly relating to the variabilities at the genetic level. A mature respiratory system entails the pivotal surfactant to promote not only lung compliance, but also anti-infection immunity in light of Surfactant Protein-A (SP-A) and Protein-D (SP-D) (figure 1). Diversities may also occur in the genes regulating SP-A and SP-D. This review hence aims to investigate multiple studies reporting SP-A and SP-D genetic variations in childhood RSV infections.

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Abstract OP-021 Figure 1

Structures of Surfactant Protein-A (SP-A) and Protein-D (SP-D). Structures of Surfactant Protein-A (SP-A) and Protein-D (SP-D). The figure outlines both the SP-A and SP-D in the monomeric units and their higher oligomeric units assembled from multiple individual monomers.

Material and Method Literature searching was independently performed using PubMed, Embase, CENTRAL, and Scopus databases until December 2023. The shortlisted studies were human-based clinical studies statistically reporting the relevance of SP-A and/or SP-D genetic analysis with childhood RSV infections.

Results Out of 1,811 studies screened, there were identified 5 (2 case-control, 2 prospective, 1 single-group) and 2 case-control full-text articles reporting SP-A and SP-D genetic variants, respectively. Regarding SP-A, the presentation of alleles 1A0, 1A2 and 6A2, genotypes 1A01A0 and 1A01A3, and Single Nucleotide Polymorphisms (SNPs) at amino acid (aa) position 19 (rs1059047) and 91 (rs17886395) were mostly mentioned as related to RSV infections, either protective or posing risks (table 1). Furthermore, the heterozygous genotype 1A01A3 transmission is reportedly linked to more severe diseases. Meanwhile, for SP-D, variations in alleles and genotypes associated with aa at positions 11 and 160 were frequently highlighted where genotype Thr160Thr was reportedly higher in RSV-infected children.

The table displays genetic variants for both SP-A and SP-D that could be raised as potential variants to explore further as these potentially demonstrate either protective or posing risk to RSV infections in infants.

Conclusions Alleles 1A0 and 6A2 for SP-A1 and SP-A2, respectively, seemed overrepresented in RSV-infected children where heterozygosity of SP-A2 genotype 1A01A3 potentially affected disease severity. Moreover, SP-D genotype Thr160Thr appeared overrepresented in RSV-infected children. Due to limited data and lack of study homogeneities, meta-analysis synthesis was unlikely and more research on SP-A and SP-D genetic aspects in RSV infections is still warranted.