高致病性韩国血统BPRRSV-2的免疫病理特征:对毒性指标和宿主免疫反应的洞察
Gyeong-Seo Park1,2, Seung-Chai Kim1, Hwan-Ju Kim1
1Collenge of Veterinary Medicine, Jeonbuk National University, Iksan, Republic of Korea.
Frontiers in immunology
|July 3, 2025
概括
两种韩国猪生殖和呼吸系统综合征病毒-2 (PRRSV-2) 菌株,GGYC45和PJ10,表现出不同的毒性和免疫抑制. PJ10导致高死亡率和严重病变,而这两种菌株都增加了免疫检查点,阻碍了T细胞的激活.
科学领域:
- 兽医病毒学 兽医病毒学
- 免疫病理学 免疫病理学
- 猪病 猪病 是一种疾病.
背景情况:
- 猪生殖和呼吸系统综合征病毒 (PRRSV) 是猪生产的主要经济威胁.
- 遗传多样性和PRRSV,特别是PRRSV-2的血统特异性致病性使疾病控制复杂化.
- 尽管有疫苗接种努力,但在韩国仍然存在明显的PRRSV-2血统.
研究的目的:
- 为了比较两个韩国血统B (LKB) PRRSV-2菌株 (GGYC45和PJ10) 的免疫病理特征.
- 评估这些LKB菌株诱导的毒性和免疫反应与类似疫苗菌株 (M8) 相比.
主要方法:
- 三十只4周大的小猪被试验感染了PRRSV-2菌株 (M8,GGYC45,PJ10) 或对照.
- 监测了临床症状,体重增加和病毒载量.
- 组织病理学,支气管支气管洗 (BAL) 细胞分析,流动细胞计和免疫检查点分子表达被评估在感染后的12天和28天.
主要成果:
- PRRSV-2菌株GGYC45和PJ10引起中度至重度的临床症状.
- PJ10感染导致高死亡率,减轻体重增加,高病毒血量和严重的呼吸/神经病变.
- 这两种LKB菌株都在BAL细胞中增加了免疫检查点分子 (PD1,PDL1,CTLA4,IDO1,LAG3),损害了T细胞激活.
结论:
- 遗传上不同的PRRSV-2菌株在猪中表现出差异性的毒性和免疫调节作用.
- 提高免疫检查点表达是PRRSV诱导的免疫抑制和持久性的关键机制.
- 控制策略必须考虑PRRSV的遗传异质性和免疫逃避.
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