Cafruny W A, Strancke C R, Kowalchyk K, Plagemann P G
J Gen Virol. 1986 Jan;67 ( Pt 1):27-37. doi: 10.1099/0022-1317-67-1-27.
Infection with the lactate dehydrogenase-elevating virus (LDV) triggers a generally fatal paralytic disease in old immunosuppressed C58 mice, but not in comparable mice of many other strains. We have compared the replication of LDV and the humoral immune response to it in C58 mice and mice of various resistant strains. Plasma LDV titres of persistently infected C58 mice were about tenfold higher than in other strains of mice and the proportion of LDV-permissive macrophages in peritoneal exudates of C58 mice was about twice as high as that observed in other mouse strains. C58 mice developed normal levels of anti-LDV IgG, as measured by ELISA, and normal levels of IgG that sensitized LDV to neutralization by rabbit anti-mouse IgG. C58 mice also developed normal IgM and IgG responses to human gamma-globulin and sheep erythrocytes. The antibody responses to LDV were similarly inhibited by cyclophosphamide in C58 and resistant strains of mice, which enhanced the incidence of signs of paralysis only in C58 mice. Thus, the sensitivity of C58 mice to LDV-induced paralytic disease is not due to an inherent inability of the mice to mount a humoral antibody response to LDV, and a suppression of the antibody response by cyclophosphamide is not the only prerequisite for development of the disease. We have quantified LDV in various tissues of immunosuppressed and non-immunosuppressed, 8- or 9-month-old C58 mice as a function of time after LDV infection and in relation to the development of paralytic disease. Changes in tissue LDV titres as a function of time after infection paralleled those found in the plasma; LDV titres were highest 1 day post-infection, and then decreased to a lower persistent level during the next 1 to 2 weeks. Tissue LDV titres, including those of the spinal cord, were lower than those in the plasma, and our results indicate that most of the LDV in tissue homogenates may be attributable to blood contamination, even though the animals were extensively perfused before removal of the tissues.
感染乳酸脱氢酶升高病毒（LDV）会在年老的免疫抑制C58小鼠中引发一种通常致命的麻痹性疾病，但在许多其他品系的类似小鼠中则不会。我们比较了C58小鼠和各种抗性品系小鼠中LDV的复制情况以及对其的体液免疫反应。持续感染的C58小鼠的血浆LDV滴度比其他品系小鼠高约十倍，C58小鼠腹腔渗出液中对LDV敏感的巨噬细胞比例约为其他小鼠品系的两倍。通过ELISA检测，C58小鼠产生的抗LDV IgG水平正常，使LDV对兔抗小鼠IgG中和敏感的IgG水平也正常。C58小鼠对人γ-球蛋白和绵羊红细胞也产生正常的IgM和IgG反应。在C58小鼠和抗性品系小鼠中，环磷酰胺对LDV抗体反应的抑制作用相似，而环磷酰胺仅在C58小鼠中增加了麻痹症状的发生率。因此，C58小鼠对LDV诱导的麻痹性疾病的敏感性并非由于小鼠自身无法对LDV产生体液抗体反应，环磷酰胺对抗体反应的抑制也不是该疾病发生发展的唯一先决条件。我们对免疫抑制和未免疫抑制的8或9月龄C58小鼠在感染LDV后的不同时间以及与麻痹性疾病发展相关的各种组织中的LDV进行了定量。感染后不同时间组织中LDV滴度的变化与血浆中的变化相似；感染后1天LDV滴度最高，然后在接下来的1至2周内降至较低的持续水平。包括脊髓在内的组织LDV滴度低于血浆中的滴度，我们的结果表明，即使在取出组织前对动物进行了广泛灌注，组织匀浆中的大多数LDV可能仍归因于血液污染。
