Abstract

Respiratory syncytial virus (RSV) infections have a high prevalence in young children, immunocompromised adults, and elderly, raising global concerns. Global RSV surveillance infers an 8%–27% mortality rate in preterm-born children, with 2.8 million/year. Continuous surveillance studies, coupled with molecular epidemiological investigations, are essential to comprehend the virus’s evolutionary dynamics and devise effective preventive strategies. The study investigates the evolutionary dynamics and molecular characterization of the RSV F-protein using bioinformatic pipelines on NCBI and GISAID data sets and molecular analysis of clinical specimens collected from children. We found S255N/G, N262S, N268I, K272M/N, and S275F/A mutations in the heptad repeat region “A” that were associated with inducing resistance toward palivizumab from bioinformatics analysis of surveillance data sets. Molecular characterization of RSV F protein from clinical specimens found L45F mutations responsible for forming new clades, L172Q and S173L substitutions for suptavumab resistance, and N276S mutations for potentially impacting palivizumab resistance. Six N-glycosylation sites are found at 27, 70, 116, 120, 126, and 500 in all RSV strains. Purifying selection, maintaining fusion protein stability, was observed. Phylogenetic analysis reveals genetic variability, with RSV B showing higher diversity than RSV A, forming distinctive clades belonging to B.D (BA9) and A.D (ON1) strains of RSV B and A, respectively. The phylodynamics of RSV indicate a uniform increase in effective population size. Understanding the F protein’s structure and dynamics is essential for elucidating the virus’s pathogenic mechanisms and developing effective vaccines and antiviral therapies.