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麻疹病毒感染中的免疫损伤。II. 通过抗原调节抑制免疫损伤。

Immunologic injury in measles virus infection. II. Suppression of immune injury through antigenic modulation.

作者信息

Joseph B S, Oldstone M B

出版信息

J Exp Med. 1975 Oct 1;142(4):864-76. doi: 10.1084/jem.142.4.864.

Abstract

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.

摘要

在向麻疹病毒中添加抗体后,感染细胞表面表达的麻疹病毒抗原在体外可从细胞膜上被调节。从细胞表面去除麻疹病毒抗原的过程相对较快,同时抗体和补体裂解这些细胞的能力也会相应降低。表面病毒抗原的调节可在无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。急性感染细胞长时间暴露于麻疹病毒抗体中会导致一群细胞呈现正常的细胞形态和生长行为。这些细胞在内部继续表达麻疹病毒抗原,但不在细胞表面表达,并且对免疫裂解具有抗性。一旦去除抗病毒抗体,麻疹病毒抗原会再次出现在细胞表面,出现巨细胞和多核细胞形成,随后细胞死亡。这些观察结果可能解释了在人类某些慢性感染中,尽管宿主有强烈的抗病毒免疫反应,病毒仍会持续存在的现象。

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