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首页> 美国卫生研究院文献>Journal of Virology >Pseudorabies virus glycoprotein gIII is a major target antigen for murine and swine virus-specific cytotoxic T lymphocytes.
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Pseudorabies virus glycoprotein gIII is a major target antigen for murine and swine virus-specific cytotoxic T lymphocytes.

机译：伪狂犬病病毒糖蛋白gIII是鼠和猪病毒特异性细胞毒性T淋巴细胞的主要靶抗原。

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Pseudorabies virus (PrV) is the etiological agent of Aujeszky's disease, a disease that causes heavy economic losses in the swine industry. A rational approach to the generation of an effective vaccine against this virus requires an understanding of the immune response induced by it and of the role of the various viral antigens in inducing such a response. We have constructed mutants of PrV [strain PrV (Ka)] that differ from each other only in expression of the viral nonessential glycoproteins gI, gp63, gX, and gIII (i.e., are otherwise isogenic). These mutants were used to ascertain the importance of each of the nonessential glycoproteins in eliciting a PrV-specific cytotoxic T-lymphocyte (CTL) response in mice and pigs. Immunization of DBA/2 mice and pigs with a thymidine kinase-deficient (TK-) mutant of PrV elicits the formation of cytotoxic cells that specifically lyse syngeneic infected target cells. These PrV-specific cytolytic cells have the phenotype of major histocompatibility complex class I antigen-restricted CTLs. The relative number of CTLs specific for glycoproteins gI, gp63, gX, and gIII induced in mice vaccinated with a TK- mutant of PrV was ascertained by comparing their levels of cytotoxicity against syngeneic cells infected with either wild-type virus or gI-/gp63-, gX-, or gIII- virus deletion mutants. The PrV-specific CLTs were significantly less effective in lysing gIII(-)-infected targets than in lysing gI-/gp63-, gX-, or wild-type-infected targets. The in vitro secondary CTL response of lymphocytes obtained from either mice or pigs 6 or more weeks after immunization with a TK- mutant of PrV was also tested. Lymphocytes obtained from these animals were cultured with different glycoprotein-deficient mutants of PrV, and their cytolytic activities against wild-type-infected targets were ascertained. The importance of each of the nonessential viral glycoproteins in eliciting CTLs was assessed from the effectiveness of each of the virus mutants to stimulate the secondary anti-PrV CTL response. Cultures of both murine or swine lymphocytes that had been stimulated with gIII- virus contained only approximately half as many lytic units as did those stimulated with either wild-type virus, a gX- virus mutant, or a gI-/gp63- virus mutant. Thus, a large proportion of the PrV-specific CTLs that are induced by immunization with PrV of both mice and pigs are directed against gIII. Furthermore, glycoproteins gI, gp63, and gX play at most a minor role in the CTL response of these animals to PrV.
机译：伪狂犬病病毒（PrV）是Aujeszky病的病原体，该病在养猪业中造成严重的经济损失。产生针对这种病毒的有效疫苗的合理方法需要了解由其诱导的免疫应答以及各种病毒抗原在诱导这种应答中的作用。我们已经构建了仅在病毒非必需糖蛋白gI，gp63，gX和gIII的表达上彼此不同的PrV [PrV（Ka）菌株]突变体（即是同基因的）。这些突变体用于确定每种非必需糖蛋白在引起小鼠和猪的PrV特异性细胞毒性T淋巴细胞（CTL）反应中的重要性。用PrV的胸苷激酶缺陷型（TK-）突变体对DBA / 2小鼠和猪进行免疫接种会引起细胞毒性细胞的形成，该细胞毒性细胞会特异性裂解同源感染的靶细胞。这些PrV特异性溶细胞具有主要组织相容性复合物I类抗原限制性CTL的表型。通过比较它们对被野生型病毒或gI- / gp63感染的同系细胞的细胞毒性水平，可以确定在用PrV TK突变株接种的小鼠中诱导的糖蛋白gI，gp63，gX和gIII特异的CTL的相对数量。 -，gX-或gIII-病毒缺失突变体。 PrV特异的CLTs在溶解gIII（-）感染的靶标上比溶解gI- / gp63-，gX-或野生型感染的靶标的效果明显差。还测试了用PrV的TK突变体免疫后6周或更长时间从小鼠或猪获得的淋巴细胞的体外次级CTL应答。用不同的糖蛋白缺陷型PrV突变株培养从这些动物获得的淋巴细胞，并确定它们对野生型感染靶标的溶细胞活性。从每个病毒突变体刺激次级抗PrV CTL反应的有效性评估了每个非必需病毒糖蛋白在引发CTL中的重要性。用gIII-病毒刺激的鼠或猪淋巴细胞的培养物，其裂解单位只有野生型病毒，gX-病毒突变体或gI- / gp63-病毒突变体刺激的裂解单位的一半。因此，小鼠和猪的PrV免疫诱导的大部分PrV特异性CTL都针对gIII。此外，糖蛋白gI，gp63和gX在这些动物对PrV的CTL反应中最多只发挥次要的作用。

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