PRIMING FOR LOCAL AND SYSTEMIC ANTIBODY MEMORY RESPONSES TO BOVINE RESPIRATORY SYNCYTIAL VIRUS - EFFECT OF AMOUNT OF VIRUS, VIRUS-REPLICATION, ROUTE OF ADMINISTRATION AND MATERNAL ANTIBODIES
PRIMING FOR LOCAL AND SYSTEMIC ANTIBODY MEMORY RESPONSES TO BOVINE RESPIRATORY SYNCYTIAL VIRUS - EFFECT OF AMOUNT OF VIRUS, VIRUS-REPLICATION, ROUTE OF ADMINISTRATION AND MATERNAL ANTIBODIES
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DOI：
10.1016/0165-2427(89)90057-3
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发表时间：
1989-09-01
影响因子：
1.8
通讯作者：
STRAVER, PJ
中科院分区：
文献类型：
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作者：
KIMMAN, TG;WESTENBRINK, F;STRAVER, PJ
我们研究了小牛能够针对牛呼吸道合胞病毒（BRSV）引发黏膜和血清抗体记忆反应的条件，以及这些反应与对该病毒的防护之间的关系。小牛通过呼吸道接种低剂量或高剂量的活病毒、灭活病毒进行免疫激发，或者通过肌肉注射活病毒。小牛通过呼吸道进行攻毒。通过呼吸道用活病毒进行免疫激发可在血清和黏膜上诱导出初次抗体反应，低剂量和高剂量病毒激发后的反应相同。这些反应受到母源抗体的抑制。对血清阴性的小牛进行肌肉内免疫激发可诱导出血清IgG1反应，有时还可诱导出血清IgM和IgG2反应，但在黏膜上未检测到反应。通过肌肉注射或呼吸道途径免疫激发的小牛血清可识别相同的病毒蛋白。用灭活病毒免疫激发后，或者对具有母源抗体的小牛进行肌肉内免疫激发后，均未观察到反应。攻毒后，通过呼吸道用活病毒免疫激发过的小牛产生了黏膜和血清抗体记忆反应，无论其是否具有母源抗体。一头饲喂初乳的小牛表现出黏膜记忆反应，尽管血清反应仍受到母源抗体的抑制。经过这样免疫激发的小牛在攻毒后均未排出病毒。肌肉内免疫激发也能在攻毒后引发黏膜和血清记忆反应，然而这些反应可能开始得稍晚一些，并且与防止病毒排出无关。用灭活病毒进行免疫激发，或者在存在母源抗体的情况下通过肌肉注射活病毒，在诱导记忆和防止病毒排出方面被证明是最无效的。因此，通过呼吸道用活病毒进行免疫激发可使具有和不具有母源抗体的小牛都获得防止病毒排出的保护。这种保护与强烈且快速的黏膜抗体记忆反应相关，但反之不一定成立。在攻毒时，防止病毒排出与血清中和抗体、血清IgG1或鼻腔IgA抗体的滴度无关。
We studied the conditions under which calves can be primed for mucosal and serum antibody memory responses against bovine respiratory syncytial virus (BRSV), and the relationship between such responses and protection against the virus. Calves were primed via the respiratory tract with a low or high amount of live virus, with killed virus, or intramuscularly with live virus. Calves were challenged via the respiratory tract. Priming with live virus via the respiratory tract induced primary antibody responses in serum and on the mucosae, which were identical after the low and the high amount of virus. These responses were suppressed by maternal antibodies. Intramuscular priming of seronegative calves induced serum IgG1 and sometimes serum IgM and IgG2 responses, but no responses were detected on the mucosae. Sera of calves primed by the intramuscular or the respiratory route recognized the same viral proteins. No responses were observed after priming with killed virus, or after intramuscular priming of calves with maternal antibodies. After challenge, mucosal and serum antibody memory responses developed in calves that had been primed via the respiratory tract with live virus, whether they had maternal antibodies or not. One colostrum-fed calf showed a mucosal memory response, although serum responses were still suppressed by maternal antibodies. None of the calves thus primed shed virus after challenge. Intramuscular priming also primed for mucosal and serum memory responses after challenge, which however started perhaps slightly later and were not associated with protection against virus shedding. Priming with killed virus, or with liver virus intramuscularly in the presence of maternal antibodies proved least effective in inducing memory and protection against virus shedding. Thus, protection against virus shedding was afforded by priming with live virus via the respiratory tract, both in calves with an without maternal antibodies. Protection was associated with a strong and rapid mucosal antibody memory response, but the reverse was not necessarily true. Protection against virus excretion had no relationship to titers of serum neutralizing or serum IgG1 or nasal IgA antibodies at the time of challenge.