Spiller O B, Hanna S M, Devine D V, Tufaro F
Department of Pathology, University of British Columbia, and Canadian Red Cross Society Blood Services, Vancouver Center.
J Infect Dis. 1997 Aug;176(2):339-47. doi: 10.1086/514050.
Complement provides a key immunologic defense against invading pathogens; thus, a clear understanding of the interactions between cytomegalovirus (CMV) and complement may permit the development of strategies to enhance CMV neutralization. In the presence of specific anti-CMV antibodies, complement enhanced the neutralizing ability of serum by 2- to 3-fold. However, in the absence of specific anti-CMV antibodies, complement was ineffective in neutralizing CMV virions by plaque assay. Although complement alone did not mediate any neutralizing effect, CMV consumed complement activity from seronegative serum, resulting in the deposition of C3 on the virion. However, only in the presence of specific anti-CMV antibody did complement activation continue to the deposition of C9 on the virions. These results strongly suggest complement regulation by CMV virions that is modulated by anti-CMV antibody; this regulation may be attributed to three host complement regulators on the virions: CD55, CD46, and CD59.
补体提供了针对入侵病原体的关键免疫防御；因此，清楚了解巨细胞病毒（CMV）与补体之间的相互作用可能有助于制定增强CMV中和作用的策略。在存在特异性抗CMV抗体的情况下，补体可使血清的中和能力提高2至3倍。然而，在不存在特异性抗CMV抗体的情况下，通过噬斑测定法，补体在中和CMV病毒粒子方面无效。虽然单独的补体不介导任何中和作用，但CMV消耗了血清阴性血清中的补体活性，导致C3沉积在病毒粒子上。然而，只有在存在特异性抗CMV抗体的情况下，补体激活才会持续到C9沉积在病毒粒子上。这些结果强烈表明CMV病毒粒子对补体的调节作用受到抗CMV抗体的调节；这种调节可能归因于病毒粒子上的三种宿主补体调节因子：CD55、CD46和CD59。
