Pathogenicity of genotype 2.1 classical swine fever virus isolated from Japan in 2019 in pigs.

Classical swine fever (CSF) re-emerged in Japan in 2018 for the first time in 26 years. The disease has been known to be caused by a moderately pathogenic virus, rather than the highly pathogenic virus that had occurred in the past. However, the underlying pathophysiology remains unknown. This study conducted an experimental challenge on specific pathogen-free (SPF) pigs in a naïve state for 2, 4, and 6 weeks and confirmed the disease state during each period by clinical observation, virus detection, and pathological necropsy. We revealed the pathological changes and distribution of pathogens and virus-specific antibodies at each period after virus challenge. These results were comprehensively analyzed and approximately 70% of the pigs recovered, especially at 4- and 6-week post-virus challenge. This study provides useful information for future countermeasures against CSF by clarifying the pathogenicity outcomes in unvaccinated pigs with moderately pathogenic genotype 2.1 virus.

The formation process of button ulcers in pigs experimentally infected with a subgenotype 2.1 isolate of classical swine fever virus.

We evaluated the role of classical swine fever virus (CSFV) in the formation of button ulcers in the mucosa of the gastrointestinal tract. Histopathological and immunohistochemical analyses of pigs experimentally infected with a subgenotype 2.1 isolate of CSFV, which was isolated in Japan in 2019, revealed follicular necrosis in the submucosal mucosa-associated lymphoid tissue and herniation of crypts as factors that contribute to the development of button ulcers during CSFV infection. These findings indicate that CSFV induces follicular necrosis and is one of the causative agents of button ulcers in pigs.