Nguyen L, Knipe D M, Finberg R W
Laboratory of Infectious Diseases, Dana-Farber Cancer Institute, Boston, MA 02115.
J Immunol. 1994 Jan 15;152(2):478-84.
Infection of mice with live viruses leads to a dramatic increase in the amount of IgG2a Ig with a consequent shift in the ratio of IgG1/IgG2a. To examine the Ig subclass shift induced by viral infection, we challenged mice with live virus, inactivated virus, or replication-defective mutant viruses that were able to infect cells and produce some viral proteins but were not able to complete a replicative cycle. While killed (or inactivated) virus was capable of inducing HSV-specific antibody, it did not stimulate a shift in the subclass of the total Ig. Replication-defective mutant viruses that fail to express a functional ICP8 or ICP27 protein, but not a mutant expressing a defective ICP4 protein, were able to stimulate the shift. Thus, only a portion of the lytic cycle is sufficient to induce the shift. At least part of the effect is mediated by IFN-gamma.
用活病毒感染小鼠会导致IgG2a Ig量急剧增加，从而使IgG1/IgG2a的比例发生变化。为了研究病毒感染诱导的Ig亚类转换，我们用活病毒、灭活病毒或复制缺陷型突变病毒攻击小鼠，这些突变病毒能够感染细胞并产生一些病毒蛋白，但无法完成复制周期。虽然灭活病毒能够诱导HSV特异性抗体，但它不会刺激总Ig亚类的转换。无法表达功能性ICP8或ICP27蛋白的复制缺陷型突变病毒，而不是表达缺陷型ICP4蛋白的突变病毒，能够刺激这种转换。因此，只有部分裂解周期足以诱导这种转换。至少部分效应是由IFN-γ介导的。
