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抗体对慢病毒复制的调节作用。针对山羊关节炎-脑炎病毒的非中和性抗体可增强巨噬细胞感染的早期阶段,但不会导致病毒粒子产量增加。

Modulation of lentivirus replication by antibodies. Non-neutralizing antibodies to caprine arthritis-encephalitis virus enhance early stages of infection in macrophages, but do not cause increased production of virions.

作者信息

Jolly P E, Huso D, Hart G, Narayan O

机构信息

Division of Comparative Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205.

出版信息

J Gen Virol. 1989 Aug;70 ( Pt 8):2221-6. doi: 10.1099/0022-1317-70-8-2221.

DOI:10.1099/0022-1317-70-8-2221
PMID:2549189
Abstract

Non-neutralizing antibodies to caprine arthritis-encephalitis virus (CAEV) enhance the early stages of the virus life cycle but do not potentiate enhanced production of virus particles by macrophages. In primary macrophages used for these studies, there was enhancement in binding, internalization and uncoating of virus pretreated with non-neutralizing sera in comparison to virus pretreated with a non-immune serum. However, this did not lead to enhanced production of virus particles. Failure of non-neutralizing sera to inactivate CAEV may be due in part to low avidity of the antibodies for the virus particles which contain sialic acids on their envelopes, because desialylation of the particles made them neutralizable. The non-neutralizing antibodies probably bound to most of the native virus particles which were then internalized via Fc receptor-mediated endocytosis and degraded. Sialylated particles that failed to bind antibodies probably caused the infection. Thus there was no true enhancement of infection. The previously reported increase in severity of lesions in animals immunized with inactivated CAEV particles prior to challenge with live virus suggested enhancement of infection but in the light of our finding this may have been caused by factors other than an increase in production in the number of infectious virus particles.

摘要

抗山羊关节炎-脑炎病毒(CAEV)的非中和抗体可增强病毒生命周期的早期阶段,但不会增强巨噬细胞产生病毒颗粒的能力。在用于这些研究的原代巨噬细胞中,与用非免疫血清预处理的病毒相比,用非中和血清预处理的病毒在结合、内化和脱壳方面有所增强。然而,这并未导致病毒颗粒产生的增加。非中和血清无法灭活CAEV,部分原因可能是抗体对包膜上含有唾液酸的病毒颗粒亲和力较低,因为颗粒的去唾液酸化使其可被中和。非中和抗体可能与大多数天然病毒颗粒结合,然后通过Fc受体介导的内吞作用内化并降解。未能结合抗体的唾液酸化颗粒可能导致感染。因此,并没有真正增强感染。先前报道在用活病毒攻击之前用灭活的CAEV颗粒免疫的动物中病变严重程度增加,这表明感染增强,但根据我们的发现,这可能是由感染性病毒颗粒数量增加以外的因素引起的。

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