Moore D M, Cowan K M
J Gen Virol. 1978 Dec;41(3):549-62. doi: 10.1099/0022-1317-41-3-549.
Large and small plaque variants of A12 foot-and-mouth disease virus were shown to have specific antigenic determinants. Large plaque virus antigenic specificity was destroyed by trypsin treatment, but the small plaque antigen was resistant despite cleavage of the trypsin-sensitive polypeptide. The cleavage of polypeptide VP3 by trypsin resulted in the formation of a new antigen not present on untreated virus. The effects of chymotrypsin and trypsin on the polypeptides of the plaque variants have been examined and related to changes in antigenicity, infectivity, and exposure of the polypeptides at the surface of the capsid. The results are discussed in relation to the orientation of the trypsin-sensitive polypeptide in the virus capsid.
A12口蹄疫病毒的大、小斑块变异体显示具有特定的抗原决定簇。大斑块病毒的抗原特异性经胰蛋白酶处理后被破坏，但小斑块抗原尽管其胰蛋白酶敏感多肽被裂解仍具有抗性。胰蛋白酶对多肽VP3的裂解导致形成一种未处理病毒上不存在的新抗原。已研究了胰凝乳蛋白酶和胰蛋白酶对斑块变异体多肽的影响，并将其与抗原性、感染性以及多肽在衣壳表面的暴露变化相关联。根据胰蛋白酶敏感多肽在病毒衣壳中的方向对结果进行了讨论。
