Cooper N R, Nemerow G R
J Invest Dermatol. 1984 Jul;83(1 Suppl):121s-127s. doi: 10.1111/1523-1747.ep12281847.
Host defense against viral infection is extremely complex and includes both humoral and cellular immune mechanisms. This contribution examines the mechanisms by which antibody (Ab) and the complement (C) system, major constituents of the humoral immune system, inactivate viruses and block viral maturation in virus-infected cells in vitro. Ab and C may neutralize viruses by envelopment in a coating of protein, by aggregation by lysis, or by facilitating interactions with various effector cells. Ab and C molecules deposited on the surfaces of viruses may physically interfere with the ability of the virus to infect a potentially susceptible cell. This appears to be the most common mechanism by which Ab and C neutralize viruses. In rare instances, Ab and/or C may aggregate viruses; aggregation reduces the net number of infectious particles and thus is manifest as neutralization. C may lyse enveloped viruses, resulting in irreversible viral inactivation. However, this does not appear to be a major mechanism of viral neutralization. Finally, the Fc portions of bound Ab molecules as well as bound C molecules may interact with effector cells with specific receptors for these factors and thereby facilitate viral destruction. In regard to virus-infected cells, the deposition of Ab or C on the cell surface may prevent the maturation or release of viral particles and alter normal cellular functions. Ab and C may also lyse virus-infected cells, abruptly stopping further viral maturation. Such lytic events require only the F(ab')2 portion of the Ab molecule and proceed via activation of the alternative C pathway. Effector cells may also interact with Ab and/or C molecules deposited on virus-infected cells, leading to cytotoxic reactions and/or ingestion depending on the type of effector cell involved. The activated C system has the ability to produce an acute inflammatory response leading to alterations in vessel permeability, edema, changes in smooth-muscle contractility, and the influx of leukocytes. Such inflammatory responses occurring in tissues, including the skin, as a result of C activation not only retard the spread of the infection and facilitate the destruction of the infectious agent, but also in all likelihood damage normal tissues in the vicinity. In addition, C activation in tissues also has the ability to stimulate arachidonic acid metabolism and induce the release of histamine and other mediators as well as pyrogens from appropriate cell types. A number of the systemic symptoms characteristic of viral infections, such as headaches, myalgias, and fever, likely result from such processes.
机体对病毒感染的防御极其复杂，包括体液免疫和细胞免疫机制。本文探讨了抗体（Ab）和补体（C）系统（体液免疫系统的主要组成部分）在体外使病毒失活并阻止病毒在受病毒感染细胞中成熟的机制。Ab和C可通过被蛋白质包被、裂解聚集或促进与各种效应细胞的相互作用来中和病毒。沉积在病毒表面的Ab和C分子可能会物理性地干扰病毒感染潜在易感细胞的能力。这似乎是Ab和C中和病毒最常见的机制。在极少数情况下，Ab和/或C可能会使病毒聚集；聚集会减少感染性颗粒的净数量，从而表现为中和作用。C可裂解包膜病毒，导致病毒不可逆地失活。然而，这似乎并不是病毒中和的主要机制。最后，结合的Ab分子的Fc部分以及结合的C分子可能会与对这些因子具有特异性受体的效应细胞相互作用，从而促进病毒的破坏。对于受病毒感染的细胞，Ab或C在细胞表面的沉积可能会阻止病毒颗粒的成熟或释放，并改变正常的细胞功能。Ab和C也可能裂解受病毒感染的细胞，从而突然停止进一步的病毒成熟。这种裂解事件仅需要Ab分子的F(ab')2部分，并通过替代C途径的激活来进行。效应细胞也可能与沉积在受病毒感染细胞上的Ab和/或C分子相互作用，根据所涉及的效应细胞类型导致细胞毒性反应和/或吞噬作用。活化的C系统有能力产生急性炎症反应，导致血管通透性改变、水肿、平滑肌收缩性变化以及白细胞流入。由于C激活而在包括皮肤在内的组织中发生的这种炎症反应不仅会阻碍感染的传播并促进感染因子的破坏，而且很可能会损害附近的正常组织。此外，组织中的C激活还能够刺激花生四烯酸代谢，并诱导组胺和其他介质以及来自适当细胞类型的热原的释放。病毒感染的许多全身症状，如头痛、肌痛和发热，可能就是由这些过程引起的。
