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

TL;DR

This study explores how the Seoul virus evolved and how it adapts to hosts, offering insights for vaccine development.

Contribution

The study identifies seven SEOV clades and their codon usage patterns, linking host adaptation to pathogenicity.

Findings

SEOV evolved into seven clades with distinct amino acid variations and geographic clustering.

Codon usage in the S segment aligns closely with human and rat hosts, indicating strong pathogenicity.

Recombination events and selection pressures were identified in SEOV's evolutionary history.

Abstract

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.

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

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.

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

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