Cafruny W A, Chan S P, Harty J T, Yousefi S, Kowalchyk K, McDonald D, Foreman B, Budweg G, Plagemann P G
Virus Res. 1986 Sep;5(4):357-75. doi: 10.1016/0168-1702(86)90029-8.
BALB/c and Swiss mice were infected with lactate dehydrogenase-elevating virus (LDV) or immunized with glutaraldehyde-inactivated or ether-extracted virus and their plasma was monitored for anti-LDV IgG and IgM levels by ELISA and indirect fluorescent antibody staining, for neutralizing antibodies, for sensitized antibody-virus complexes, for immune complexes, and for total plasma IgG and IgM. In infected mice, anti-LDV IgM was transiently formed during the first 2 weeks post infection (p.i.) but only at a low level. Anti-LDV IgG was produced in a biphasic manner with an initial peak at about 10 days p.i. and a secondary rise reaching a maximum level 30-80 days p.i. which was retained throughout the persistent phase of infection. The concomitant appearance of comparable levels of low molecular weight immune complexes suggests that most anti-LDV IgG was complexed with LDV proteins. Also, as early as 10 days p.i., infectious antibody-LDV complexes developed, which were neutralizable by rabbit anti-mouse IgG, whereas antibodies that neutralize the infectivity of exogenously added LDV appeared only 1-2 months p.i. Throughout infection, most of the anti-LDV IgG was directed to VP-3, the envelope glycoprotein of LDV, which was found to exist in at least 10 distinct forms ranging in molecular weight from 24 to 42 kDa. Anti-LDV IgG levels as high as those observed in infected mice developed in mice immunized with inactivated LDV. Antibodies to glutaraldehyde-inactivated LDV were also mainly directed to VP-3, but exhibited no neutralizing activity. The polyclonal B cell activation associated with a persistent LDV infection and the formation of immune complexes were not observed in mice immunized with inactivated virus.
将BALB/c小鼠和瑞士小鼠感染乳酸脱氢酶升高病毒（LDV），或用戊二醛灭活或乙醚提取的病毒进行免疫，通过酶联免疫吸附测定（ELISA）和间接荧光抗体染色监测它们血浆中的抗LDV IgG和IgM水平，检测中和抗体、致敏抗体 - 病毒复合物、免疫复合物以及血浆总IgG和IgM。在感染的小鼠中，抗LDV IgM在感染后（p.i.）的前2周短暂形成，但水平较低。抗LDV IgG以双相方式产生，在感染后约10天出现初始峰值，在感染后30 - 80天出现二次上升并达到最高水平，该水平在整个感染持续期维持。低分子量免疫复合物的可比水平同时出现表明，大多数抗LDV IgG与LDV蛋白形成复合物。此外，早在感染后10天，就形成了具有感染性的抗体 - LDV复合物，其可被兔抗小鼠IgG中和，而中和外源性添加的LDV感染性的抗体在感染后1 - 2个月才出现。在整个感染过程中，大多数抗LDV IgG针对LDV的包膜糖蛋白VP - 3，发现其至少存在10种不同形式，分子量范围为24至42 kDa。在用灭活的LDV免疫的小鼠中，抗LDV IgG水平与感染小鼠中观察到的水平一样高。针对戊二醛灭活的LDV的抗体也主要针对VP - 3，但不表现出中和活性。在用灭活病毒免疫的小鼠中未观察到与持续性LDV感染相关的多克隆B细胞活化和免疫复合物的形成。
