# A Recombinant Porcine Epidemic Diarrhea Virus with Multiple S2 Subunit Mutations from China: Isolation, Genetic Characterization, and Pathogenicity Analysis

## TL;DR

A new highly virulent strain of PEDV was isolated in China and found to have multiple mutations in a key viral protein, posing a threat to pig farming.

## Contribution

Identification of a recombinant PEDV strain with multiple S2 subunit mutations and high virulence in young piglets.

## Key findings

- PEDV/FJLY202201 is a recombinant strain with mutations in the S2 subunit of the spike protein.
- The strain caused 100% mortality and significant weight loss in 3-day-old piglets.
- The virus originated from recombination events between G2a and G2b PEDV strains.

## Abstract

Porcine epidemic diarrhea virus (PEDV) is a major cause of fatal diarrhea in piglets. The continuous emergence of new variants, driven by recombination and mutation, poses a persistent global threat to the swine industry, resulting in significant economic losses. Therefore, ongoing surveillance of PEDV evolution is critical. In this study, we isolated a novel PEDV strain, designated PEDV/FJLY202201, from experimental intestinal samples collected from a diarrheal piglet in Fujian, China, and sequenced its complete genome. Complete genome analysis, phylogenetic analysis, and recombination analysis were conducted. Results showed that PEDV/FJLY202201 was a recombinant strain derived from two recombination events between G2a and G2b strains, with three breakpoints located in the ORF1b, Domain 0 (D0) and S2 subunit, respectively. Notably, multiple mutations were identified in the S2 subunit, a finding that has been rarely reported before. Furthermore, following challenge with the PEDV/FJLY202201 strain, 3-day-old piglets exhibited severe diarrhea, sustained a 30.35% weight loss, and reached 100% mortality, collectively demonstrating its high virulence. These data reveal the complex evolution of PEDV/FJLY202201 and provide a foundation for a better understanding of the genetic evolution and molecular pathogenesis of PEDV.