Immunologic injury in measles virus infection. II. Suppression of immune injury through antigenic modulation
Immunologic injury in measles virus infection. II. Suppression of immune injury through antigenic modulation
复制标题
麻疹病毒感染的免疫损伤。
DOI：
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发表时间：
1975
影响因子：
15.3
通讯作者：
M. Oldstone
中科院分区：
文献类型：
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作者：
B. Joseph;M. Oldstone
在体外添加麻疹病毒抗体后，感染细胞表面表达的麻疹病毒抗原可被细胞膜调控。从细胞表面去除麻疹病毒抗原的速度相对较快，同时伴随着抗体和补体溶解这些细胞的能力的平行降低。表面病毒抗原的调节可以在没有帽形成的情况下发生，一旦从培养基中去除麻疹病毒抗体，这种调节是完全可逆的。急性感染细胞长期暴露于麻疹病毒抗体导致细胞群表现出正常的细胞形态和生长行为。这些细胞继续在内部表达麻疹病毒抗原，而不是在细胞表面，并且对免疫裂解是难解的。一旦去除抗病毒抗体，麻疹病毒抗原再次出现在细胞表面，巨细胞和合胞体形成，细胞死亡。这些观察结果或许可以解释，在某些人类慢性感染中，尽管宿主有强烈的抗病毒免疫反应，病毒仍然存在。
Upon the addition of antibody to measles virus, measles virus antigens expressed on the surface of infected cells can be modulated from the cell's membrane in vitro. Removal of measles virus antigens from the surface of cells occurs relatively rapidly and is accompanied by a parallel reduction in the ability of antibody and complement to lyse these cells. Modulation of surface viral antigens can occur in the absence of cap formation and is fully reversible once measles virus antibodies are removed from culture medium. Protracted exposure of acutely infected cells to measles virus antibodies results in a population of cells that exhibit normal cytomorphology and growth behavior. These cells continue to express measles virus antigens internally, but not at the cell surface, and are refractory to immune lysis. Once antiviral antibody is removed, measles virus antigens again appear on the cell surface, giant cell and syncytial formation occur, and cell death follows. These observations may explain the persistence of virus in spite of a vigorous host antiviral immune response in certain chronic infections of man.