Genetic and codon usage analyses reveal the evolution of the seoul virus.

Abstract

Introduction: Seoul virus (Orthohantavirus seoulense, SEOV), a member of the Hantaviridae, causes hemorrhagic fever with renal syndrome (HFRS) through rodent hosts. However, its molecular evolutionary dynamics and codon usage patterns remain poorly understood.

Methods: This study integrated coding sequences from GenBank and previously acquired SEOV strains to systematically analyze genetic evolution and codon usage bias.

Results: It revealed that SEOV evolved seven clades (A-G) with distinct amino acid variation sites and geographic clustering. Recombination events were identified during evolution, alongside purifying and positive selection on specific sites (e.g., codon 259 in the S segment and codon 11 in the M segment). The three viral segments (L, M, and S) exhibited weak codon usage bias, predominantly driven by natural selection, with host adaptation significantly influencing evolutionary trajectories. The S segment demonstrated the strongest pathogenicity due to its closer codon usage alignment with Homo sapiens (H. sapiens) and Rattus norvegicus (R. norvegicus), whereas the L segment showed the lowest host adaptation. Divergent codon preferences among clades highlighted adaptive strategies in host-virus interactions.

Conclusion: These findings elucidate the evolutionary mechanisms of SEOV and provide a theoretical foundation for live attenuated vaccine design and region-specific viral control strategies.