Department of Veterinary Microbiology, Rajiv Gandhi Institute of Veterinary Education & Research, Puducherry, 605 009, India.
Department of Veterinary Medicine, Rajiv Gandhi Institute of Veterinary Education & Research, Puducherry, 605 009, India.
Arch Virol. 2024 Aug 27;169(9):189. doi: 10.1007/s00705-024-06096-2.
Canine parvovirus (CPV) infection causes severe gastroenteritis in canines, with high mortality in puppies. This virus evolved from feline panleukopenia virus by altering its transferrin receptor (TfR), followed by the emergence of CPV-2 variants in subsequent years with altered immunodominant amino acid residues in the VP2 protein. While previous studies have focused on the VP2 gene, there have been fewer studies on non-structural protein (NS1 and NS2) genes. In the present study, CPV genome sequences from clinical samples collected from canines throughout India in 2023, previous Indian CPV isolates from 2009-2019, and the current Indian CPV vaccine strain were compared. The study showed that the CPV-2c (N426E) variant had almost completely replaced the previously dominant CPV-2a variant (N426) in India. The Q370R mutation of VP2 was the most common change in the recent CPV-2c strain (CPV-2c 370Arg variant). Phylogenetic analysis showed the existence of three clades among the recent CPV-2c strains, and sequence analysis identified several new sites of positive selection in the VP1 (N-terminus), VP2, NS1, and NS2 protein-encoding genes in recent CPV strains, indicating the emergence of new CPV-2c variants with varied antigenic and replication properties. The predominant 'CPV-2c 370Arg variants' were grouped with the Chinese and Nigerian CPV-2c strains but were separate from the CPV vaccine strain and earlier isolates from our repository. VP2 epitope analysis predicted nine amino acid variations (including two new variations) in four potential linear B-cell epitopes in the CPV-2c 370Arg variants that might make vaccine failure more likely. This pan-Indian study lays the foundation for further research concerning the dynamics of virus evolution and understanding genetic mutations.
犬细小病毒(CPV)感染可引起犬严重的胃肠炎,幼犬死亡率很高。该病毒通过改变其转铁蛋白受体(TfR)从猫泛白细胞减少症病毒进化而来,随后在接下来的几年中出现了 CPV-2 变体,其 VP2 蛋白中的免疫优势氨基酸残基发生了改变。虽然之前的研究集中在 VP2 基因上,但对非结构蛋白(NS1 和 NS2)基因的研究较少。本研究比较了 2023 年从印度各地收集的犬临床样本、2009-2019 年之前的印度 CPV 分离株和当前的印度 CPV 疫苗株的 CPV 基因组序列。研究表明,CPV-2c(N426E)变体几乎完全取代了印度之前占主导地位的 CPV-2a 变体(N426)。VP2 的 Q370R 突变是最近 CPV-2c 株最常见的变化(CPV-2c 370Arg 变体)。系统进化分析显示,最近 CPV-2c 株存在三个分支,序列分析确定了最近 CPV 株 VP1(N 端)、VP2、NS1 和 NS2 蛋白编码基因中的几个新的正选择位点,表明具有不同抗原性和复制特性的新 CPV-2c 变体的出现。主要的“CPV-2c 370Arg 变体”与中国和尼日利亚的 CPV-2c 株聚集在一起,但与 CPV 疫苗株和我们存储库中的早期分离株分开。VP2 表位分析预测 CPV-2c 370Arg 变体的四个潜在线性 B 细胞表位中有 9 个氨基酸变异(包括两个新变异),这可能使疫苗失效的可能性更大。这项全印度研究为进一步研究病毒进化动态和遗传突变奠定了基础。