Cornelissen E, Dewerchin H L, Van Hamme E, Nauwynck H J
Laboratory of Virology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium.
Virus Res. 2009 Sep;144(1-2):285-9. doi: 10.1016/j.virusres.2009.03.017. Epub 2009 Apr 7.
Cats infected with virulent feline coronavirus which causes feline infectious peritonitis (FIP) usually succumb to disease despite high antibody concentrations. One of the mechanisms that can help resolving infection is antibody-dependent, complement-mediated lysis (ADCML) of infected cells. ADCML consists of virus-specific antibodies that bind to cell surface expressed viral proteins which result in complement activation and cell lysis. The objective of this study was to determine the sensitivity of FIP-virus (FIPV) infected cells towards ADCML and to examine the role of the accessory proteins 3abc and 7ab in this process. ADCML assays, using FIPV strain 79-1146 and its deletion mutant strain Delta 3abc/Delta 7ab, were performed on: (i) CrFK cells that show surface-expressed viral antigens, (ii) monocytes without surface-expressed viral proteins due to retention and (iii) monocytes with surface-expressed viral proteins since the antibody-mediated internalization of these proteins was blocked. As expected, no ADCML was detected of the monocytes without surface-expressed viral antigens. Surprisingly, no lysis was observed in the CrFK cells and the monocytes that do show surface-expressed viral proteins, while controls showed that the ADCML assay was functional. These experiments proof that FIPV can employ another immune evasion strategy against ADCML (besides preventing surface expression): the inhibition of complement-mediated lysis. This new evasion strategy is not attributed to the group-specific proteins since lysis of cells infected with FIPV Delta 3abc/Delta 7ab was not detected.
感染了烈性猫冠状病毒（可导致猫传染性腹膜炎，即FIP）的猫，即便抗体浓度很高，通常仍会死于该病。有助于解决感染问题的机制之一是抗体依赖性补体介导的感染细胞裂解（ADCML）。ADCML由病毒特异性抗体组成，这些抗体与细胞表面表达的病毒蛋白结合，从而导致补体激活和细胞裂解。本研究的目的是确定感染FIP病毒（FIPV）的细胞对ADCML的敏感性，并研究辅助蛋白3abc和7ab在此过程中的作用。使用FIPV毒株79 - 1146及其缺失突变株Delta 3abc/Delta 7ab进行ADCML检测，检测对象包括：（i）表面表达病毒抗原的CrFK细胞；（ii）因病毒滞留而无表面表达病毒蛋白的单核细胞；（iii）因抗体介导的这些蛋白内化被阻断而有表面表达病毒蛋白的单核细胞。正如预期的那样，未检测到无表面表达病毒抗原的单核细胞发生ADCML。令人惊讶的是，在表面表达病毒蛋白的CrFK细胞和单核细胞中未观察到裂解现象，而对照显示ADCML检测是有效的。这些实验证明FIPV可以采用另一种针对ADCML的免疫逃避策略（除了阻止表面表达之外）：抑制补体介导的裂解。这种新的逃避策略并非归因于群特异性蛋白，因为未检测到感染FIPV Delta 3abc/Delta 7ab的细胞发生裂解。
