Food Animal Health Research Program, Ohio Agricultural Research and Development Center, Department of Veterinary Preventive Medicine, The Ohio State University, Wooster, 44691, USA.
Virol J. 2012 Feb 16;9:45. doi: 10.1186/1743-422X-9-45.
Porcine reproductive and respiratory syndrome virus (PRRSV) causes chronic, economically devastating disease in pigs of all ages. Frequent mutations in the viral genome result in viruses with immune escape mutants. Irrespective of regular vaccination, control of PRRSV remains a challenge to swine farmers. In PRRSV-infected pigs, innate cytokine IFN-α is inhibited and the adaptive arm of the immunity is delayed. To elucidate both cellular and innate cytokine responses at very early stages of PRRSV infection, seven weeks old pigs maintained on a commercial pig farm were infected and analyzed.
One pig in a pen containing 25 pigs was PRRSV infected and responses from this pig and one penmate were assessed two days later. All the infected and a few of the contact neighbor pigs were viremic. At day 2 post-infection, approximately 50% of viremic pigs had greater than 50% reduction in NK cell-mediated cytotoxicity, and nearly a 1-fold increase in IFN-α production was detected in blood of a few pigs. Enhanced secretion of IL-4 (in ~90%), IL-12 (in ~40%), and IL-10 (in ~20%) (but not IFN-γ) in PRRSV infected pigs was observed. In addition, reduced frequency of myeloid cells, CD4(-)CD8(+) T cells, and CD4(+)CD8(+) T cells and upregulated frequency of lymphocytes bearing natural T regulatory cell phenotype were detected in viremic pigs. Interestingly, all viremic contact pigs also had comparable immune cell modulations.
Replicating PRRSV in both infected and contact pigs was found to be responsible for rapid modulation in NK cell-meditated cytotoxicity and alteration in the production of important immune cytokines. PRRSV-induced immunological changes observed simultaneously at both cellular and cytokine levels early post-infection appear to be responsible for the delay in generation of adaptive immunity. As the study was performed in pigs maintained under commercial environmental conditions, this study has practical implications in design of protective vaccines.
猪繁殖与呼吸综合征病毒（PRRSV）可引起各年龄段猪的慢性、具有经济破坏性的疾病。病毒基因组的频繁突变导致具有免疫逃逸突变体的病毒。无论常规接种疫苗如何，控制 PRRSV 仍然是养猪户的一大挑战。在 PRRSV 感染的猪中，先天细胞因子 IFN-α 受到抑制，免疫的适应性臂被延迟。为了阐明 PRRSV 感染早期的细胞和先天细胞因子反应，对商业养猪场饲养的 7 周龄猪进行了感染和分析。
在一个包含 25 头猪的猪圈中，一头猪被 PRRSV 感染，两天后对这头猪及其一头圈舍伙伴的反应进行了评估。所有感染的和少数接触的邻居猪都有病毒血症。感染后第 2 天，约 50%的病毒血症猪的 NK 细胞介导的细胞毒性降低了 50%以上，少数猪的 IFN-α 产量增加了近 1 倍。在 PRRSV 感染的猪中观察到 IL-4（约 90%）、IL-12（约 40%）和 IL-10（约 20%）（但不是 IFN-γ）的分泌增强。此外，在病毒血症猪中还检测到髓样细胞、CD4(-)CD8(+)T 细胞和 CD4(+)CD8(+)T 细胞的频率降低，以及携带天然 T 调节细胞表型的淋巴细胞的频率升高。有趣的是，所有病毒血症接触猪也有类似的免疫细胞调节。
在感染猪和接触猪中复制 PRRSV 被发现是导致 NK 细胞介导的细胞毒性迅速调节和重要免疫细胞因子产生改变的原因。感染后早期在细胞和细胞因子水平上同时观察到的 PRRSV 诱导的免疫变化似乎是导致适应性免疫产生延迟的原因。由于该研究是在商业环境条件下饲养的猪中进行的，因此该研究对保护性疫苗的设计具有实际意义。
Zotero 插件
