CELLULAR IMMUNE-RESPONSES OF PIGS AFTER PRIMARY INOCULATION WITH PORCINE RESPIRATORY CORONAVIRUS OR TRANSMISSIBLE GASTROENTERITIS VIRUS AND CHALLENGE WITH TRANSMISSIBLE GASTROENTERITIS VIRUS
CELLULAR IMMUNE-RESPONSES OF PIGS AFTER PRIMARY INOCULATION WITH PORCINE RESPIRATORY CORONAVIRUS OR TRANSMISSIBLE GASTROENTERITIS VIRUS AND CHALLENGE WITH TRANSMISSIBLE GASTROENTERITIS VIRUS
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DOI：
10.1016/0165-2427(94)05416-p
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发表时间：
1995-09-01
影响因子：
1.8
通讯作者：
SAIF, LJ
中科院分区：
文献类型：
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作者：
BRIM, TA;VANCOTT, JL;SAIF, LJ
在猪11日龄时经口鼻接种PRCV或TGEV后24天用TGEV攻毒的猪中，评估了细胞介导的免疫对由原发性猪呼吸道冠状病毒（PRCV）或TGEV暴露所赋予的强毒传染性胃肠炎病毒（TGEV）感染的保护性免疫的贡献。PRCV暴露诱导了仔猪对TGEV攻击的部分保护，这是基于腹泻病例数减少（42%对年龄匹配的对照猪的90%），粪便中病毒脱落有限，以及病毒中和血清抗体滴度增加;相反，所有接种TGEV的Ii日龄猪在攻击后都得到了完全保护。还对断奶猪进行了研究，以消除接触PRCV暴露母猪的泌乳免疫有助于预防TGEV的任何可能性。一旦断奶，没有PRCV暴露或年龄匹配的对照猪腹泻后TGEV的挑战，而且，两组表现出直肠病毒脱落比乳猪。在从TGEV致敏猪的肠系膜（MLN）和支气管（BLN）淋巴结制备的单核细胞中检测到强烈的淋巴细胞增殖反应（> 96 000计数/分钟（cpm））。对这些应答的分析表明，病毒特异性细胞介导的免疫应答与TGEV攻击后对直肠和鼻腔病毒脱落的保护相关。用PRCV初次接种11日龄猪，在TGEV攻击后，在哺乳和断奶猪的MLN中诱导中度、短暂的病毒特异性淋巴细胞增殖（> 47 000 cpm）。大量BLN增殖反应（> 80 000 cpm）与这些猪鼻分泌物中TGEV检测失败相关。脾脏中的病毒特异性淋巴细胞增殖延迟发作，并且幅度低于MLN和BLN中观察到的水平。毒性TGEV暴露导致T细胞亚群的百分比增加，特别是在固有层和MLN中，接近小肠中TGEV主要复制位点的粘膜相关淋巴组织。我们的研究结果证实，PRCV感染引发抗病毒免疫应答，因此，有助于对强毒TGEV攻击的部分免疫。
The contribution of cell-mediated immunity to protective immunity against virulent transmissible gastroenteritis virus (TGEV) infection conferred by primary porcine respiratory coronavirus (PRCV) or TGEV exposure was assessed in pigs that were challenged with TGEV 24 days after a primary oronasal inoculation with PRCV or TGEV when 11 days old. PRCV exposure induced partial protection against TGEV challenge in suckling pigs based upon a decreased number of diarrhea cases (42% vs. 90% in age-matched control pigs), limited virus shedding in feces, and increases in virus-neutralizing serum antibody titers; in contrast, all Ii-day-old pigs inoculated with TGEV were completely protected after challenge. Weaned pigs were also studied to eliminate any possibility that lactogenic immunity from contact PRCV-exposed sows contributed to protection against TGEV. Once weaned, none of the PRCV-exposed or age-matched control pigs had diarrhea after TGEV challenge; moreover, both groups exhibited less rectal virus shedding than suckling pigs. Vigorous lymphocyte proliferative responses (> 96 000 counts per minute (cpm)) were detected in mononuclear cells prepared from mesenteric (MLN) and bronchial (BLN) lymph nodes of TGEV-primed pigs. Analyses of these responses indicate that virus-specific cell-mediated immune responses correlated with protection against rectal and nasal virus shedding after TGEV challenge, Primary inoculation of Ii-day-old pigs with PRCV induced moderate, transient virus-specific lymphocyte proliferation (> 47 000 cpm) in MLN from both suckling and weaned pigs after TGEV challenge. Substantial BLN proliferative responses (> 80 000 cpm) correlated with failure to detect TGEV in nasal secretions from these pigs. Virus-specific lymphocyte proliferation in spleens was delayed in onset and of lower magnitude than that observed in MLN and BLN. Virulent TGEV exposure resulted in increased percentages of T cell subsets, especially in the lamina propria and MLN, mucosa-associated lymphoid tissues in proximity to the primary replication site of TGEV in the small intestine. Our results confirm that PRCV infection primes anti-viral immune responses and, thus, contributes to partial immunity against virulent TGEV challenge.