Huang, Yu LiangYu LiangHuangDeng, Ming ChungMing ChungDengTsai, Kuo JungKuo JungTsaiLiu, Hsin MengHsin MengLiuHuang, Chin ChengChin ChengHuangFUN-IN WANGCHIA-YI CHANG2023-09-182023-09-182017-01-1501681702https://scholars.lib.ntu.edu.tw/handle/123456789/635413Classical swine fever (CSF), an economically important and highly contagious disease of pigs, is caused by classical swine fever virus (CSFV). In Taiwan, CSFVs from field outbreaks belong to two distinct genotypes. The historical genotype 3.4 dominated from the 1920s to 1996, and since 1996, the newly invading genotype 2.1 has dominated. To explain the phenomenon of this virus shift in the field, representative viruses belonging to genotypes 2.1 and 3.4 were either inoculated alone (single infection) or co-inoculated (co-infection), both in vivo and in vitro, to compare the virus replication and pathogenesis. In pigs co-infected with the genotype 2.1 TD/96/TWN strain and the genotype 3.4 94.4/IL/94/TWN strain, the newly invading genotype 2.1 was detected earlier in the blood, oral fluid, and feces, and the viral loads were consistently and significantly higher than that of the historical genotype 3.4. In cell cultures, the ratio of secreted virus to cell-associated virus of the genotype 2.1 strain was higher than that of the genotype 3.4 strain. This study is the first to demonstrate a possible explanation of virus shift in the field, wherein the newly invading genotype 2.1 replicates more efficiently than did genotype 3.4 and outcompetes the replication and pathogenicity of genotype 3.4 in pigs in the field.enClassical swine fever virus | Genotype | Pathogenesis | Viral replication | Virus shift[SDGs]SDG3journal article10.1016/j.virusres.2016.11.022278896142-s2.0-84998813193https://api.elsevier.com/content/abstract/scopus_id/84998813193