Kiyohara Tomoko, Totsuka Atsuko, Yoneyama Tetsuo, Ishii Koji, Ito Toshihiro, Wakita Takaji
Department of Virology II, National Institute of Infectious Diseases, 4-7-1, Gakuen, Musashi-Murayama, Tokyo 208-0011, Japan.
Arch Virol. 2009;154(8):1263-9. doi: 10.1007/s00705-009-0433-6. Epub 2009 Jul 4.
Two anti-idiotypic monoclonal antibodies (mAb2s; named 94-2 and 94-7), were generated from a BALB/c mouse immunized with human monoclonal anti-hepatitis A virus (HAV) neutralizing antibody KF94. We characterized the properties of the mAb2s and determined interactions between mAb2s, KF94 and HAV using enzyme-linked immunosorbent assay, immunofluorescence assay and HAV infectivity assay. Inactivated HAV inhibited mAb2 binding to KF94, indicating that the mAb2s mimicked the HAV neutralization site that was complementary to the paratope of KF94. MAb2 94-7 competed with an anti-HAV cellular receptor antibody for binding to HAV-susceptible cells and partially blocked virus infection. We speculated that mAb2 94-7 mimicked a portion of the HAV receptor-binding site. The ability to generate mAb2 implies that HAV receptor-binding sites are exposed on the surface of HAV, permitting antibody access.
用人类抗甲型肝炎病毒(HAV)中和抗体KF94免疫BALB/c小鼠,产生了两种抗独特型单克隆抗体(mAb2s;命名为94 - 2和94 - 7)。我们对mAb2s的特性进行了表征,并使用酶联免疫吸附测定、免疫荧光测定和HAV感染性测定来确定mAb2s、KF94和HAV之间的相互作用。灭活的HAV抑制mAb2与KF94的结合,这表明mAb2s模拟了与KF94互补位互补的HAV中和位点。单克隆抗体94 - 7与抗HAV细胞受体抗体竞争结合HAV易感细胞,并部分阻断病毒感染。我们推测单克隆抗体94 - 7模拟了HAV受体结合位点的一部分。产生mAb2的能力意味着HAV受体结合位点暴露在HAV表面,便于抗体接近。