ArticleVirus research2023
Molecular evolutionary analyses of the fusion protein gene in human respirovirus 1.
Article in Virus research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Molecular Evolution of theMicroorganisms · 2026Article
- Molecular Evolution of theMicroorganisms · 2025Article
- Phylogenomic Analyses of the Hemagglutinin-Neuraminidase (Microorganisms · 2025Article
- Molecular Evolutionary Analyses of the Fusion Genes in Human Parainfluenza Virus Type 4.Microorganisms · 2024Article
- Molecular Evolutionary Analyses of the Spike Protein Gene and Spike Protein in the SARS-CoV-2 Omicron Subvariants.Microorganisms · 2023Article
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Few evolutionary studies of the human respiratory virus (HRV) have been conducted, but most of them have focused on HRV3. In this study, the full-length fusion (F) genes in HRV1 strains collected from various countries were subjected to time-scaled phylogenetic, genome population size, and selective pressure analyses. Antigenicity analysis was performed on the F protein. The time-scaled phylogenetic tree using the Bayesian Markov Chain Monte Carlo method estimated that the common ancestor of the HRV1 F gene diverged in 1957 and eventually formed three lineages. Phylodynamic analyses showed that the genome population size of the F gene has doubled over approximately 80 years. Phylogenetic distances between the strains were short (< 0.02). No positive selection sites were detected for the F protein, whereas many negative selection sites were identified. Almost all conformational epitopes of the F protein, except one in each monomer, did not correspond to the neutralising antibody (NT-Ab) binding sites. These results suggest that the HRV1 F gene has constantly evolved over many years, infecting humans, while the gene may be relatively conserved. Mismatches between computationally predicted epitopes and NT-Ab binding sites may be partially responsible for HRV1 reinfection and other viruses such as HRV3 and respiratory syncytial virus.
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