Animal Health Research Institute, Council of Agriculture, Executive Yuan, 376 Chung-Cheng Road, Tansui, New Taipei City 25158, Taiwan.
School of Veterinary Medicine, National Taiwan University, No. 1, Section 4, Roosevelt Road, Taipei 10617, Taiwan.
Viruses. 2020 Dec 2;12(12):1378. doi: 10.3390/v12121378.
Porcine epidemic diarrhea virus (PEDV) causes severe diarrhea and a high rate of mortality in suckling pigs. The epidemic of PEDV that occurred after 2013 was caused by non-insertion and deletion of S gene (S-INDEL) PEDV strains. During this epidemic, a variant of the non-S-INDEL PEDV strain with a large deletion of 205 amino acids on the spike gene (5-17-V) was also found to co-exist with a non-S-INDEL PEDV without deletion (5-17-O). Herein, we describe the differences in the complete genome, distribution, virulence, and antigenicity between strain 5-17-O and variant strain 5-17-V. The deletion of 205 amino acids was primarily located in the S1 domain and was associated with milder clinical signs and lower mortality in suckling pigs than those of the 5-17-O strain. The 5-17-V strain-induced antibody did not completely cross-neutralize the 5-17-O strain. In conclusion, the deletion in the S1 region reduces the virulence of PEDV and influences the virus-neutralizing activities of the antibody it induces.
猪流行性腹泻病毒（PEDV）可引起仔猪严重腹泻和高死亡率。2013 年后发生的 PEDV 流行是由 S 基因非插入缺失（S-INDEL）PEDV 株引起的。在此期间，还发现一种 Spike 基因上 205 个氨基酸缺失的非 S-INDEL PEDV 变异株（5-17-V）与无缺失的非 S-INDEL PEDV（5-17-O）共同存在。在此，我们描述了 5-17-O 株和变异株 5-17-V 之间在全基因组、分布、毒力和抗原性方面的差异。205 个氨基酸的缺失主要位于 S1 结构域，与 5-17-O 株相比，仔猪的临床症状较轻，死亡率较低。5-17-V 株诱导的抗体不能完全中和 5-17-O 株。总之，S1 区的缺失降低了 PEDV 的毒力，并影响了其诱导的抗体的病毒中和活性。
