ALEUTIAN MINK DISEASE PARVOVIRUS INFECTION OF MINK MACROPHAGES AND HUMAN MACROPHAGE CELL-LINE U937 - DEMONSTRATION OF ANTIBODY-DEPENDENT ENHANCEMENT OF INFECTION
ALEUTIAN MINK DISEASE PARVOVIRUS INFECTION OF MINK MACROPHAGES AND HUMAN MACROPHAGE CELL-LINE U937 - DEMONSTRATION OF ANTIBODY-DEPENDENT ENHANCEMENT OF INFECTION
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DOI：
10.1128/jvi.67.12.7017-7024.1993
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发表时间：
1993-12-01
影响因子：
5.4
通讯作者：
BLOOM, ME
中科院分区：
文献类型：
--
作者：
KANNO, H;WOLFINBARGER, JB;BLOOM, ME
水貂阿留申病细小病毒（ADV）感染成年水貂的巨噬细胞。毒性ADV-Utah I株，而不是细胞培养适应的ADV-G株，在体外感染水貂腹腔巨噬细胞培养物和人巨噬细胞系U937。然而，ADV-G与ADV感染的貂血清预孵育增强了其对U937细胞的感染性。增强活性存在于血清中蛋白A结合免疫球蛋白G组分中，但F（ab '）2片段不能增强感染。另一方面，相同的血清抑制ADV-G感染的Crandell猫肾（CRFK）细胞。尽管U937细胞不完全允许抗体增强的ADV-G感染，但ADV mRNA表达、基因组扩增和蛋白质表达与先前发现的ADV-Utah I感染U937细胞的情况相同。ADV-Utah I与可溶性蛋白A预孵育可部分抑制U937细胞的感染，但不影响CRFK细胞的感染。在水貂腹腔巨噬细胞中，用感染的水貂血清预孵育不会使ADV-G具有感染性。然而，无抗体的ADV-Utah I从感染的新生水貂试剂盒制备的水貂巨噬细胞的感染性被ADV感染的水貂血清增强。此外，蛋白A部分阻断ADV-Utah I感染水貂巨噬细胞培养物。这些结果表明ADV-Utah I通过Fc受体介导的机制进入貂巨噬细胞和U937细胞。这种抗体依赖性增强的机制也可能有助于体内ADV感染。此外，由于水貂ADV感染的特征是过量产生抗ADV免疫球蛋白，因此抗体依赖性增强可能在体内ADV持续感染的建立中起关键作用。
Aleutian mink disease parvovirus (ADV) infects macrophages in adult mink. The virulent ADV-Utah I strain, but not the cell culture-adapted ADV-G strain, infects mink peritoneal macrophage cultures and the human macrophage cell line U937 in vitro. However, preincubation of ADV-G with ADV-infected mink serum enhanced its infectivity for U937 cells. The enhancing activity was present in the protein A-binding immunoglobulin G fraction in the serum, but F(ab')2 fragments failed to enhance the infection. On the other hand, the same sera inhibited ADV-G infection of Crandell feline kidney (CRFK) cells. Although U937 cells were not fully permissive for antibody-enhanced ADV-G infection, ADV mRNA expression, genome amplification, and protein expression were identical to those found previously for ADV-Utah I infection of U937 cells. Preincubation of ADV-Utah I with soluble protein A partly inhibited the infection of U937 cells but did not affect infection of CRFK cells. In mink peritoneal macrophages, preincubation with the infected mink serum did not make ADV-G infectious. However, the infectivity for mink macrophages of antibody-free ADV-Utah I prepared from the lungs of infected newborn mink kits was enhanced by ADV-infected mink serum. Moreover, protein A partly blocked ADV-Utah I infection of mink macrophage cultures. These results suggested that ADV-Utah I enters mink macrophages and U937 cells via an Fc receptor-mediated mechanism. This mechanism, antibody-dependent enhancement, may also contribute to ADV infection in vivo. Furthermore, since ADV infection in mink is characterized by overproduction of anti-ADV immunoglobulins, antibody-dependent enhancement may play a critical role in the establishment of persistent infection with ADV in vivo.