PATHOGENESIS OF ALEUTIAN MINK DISEASE PARVOVIRUS INFECTIONS

阿留申水貂病细小病毒感染的发病机制

• 批准号: 6431513
• 负责人: Marshall Elliott Bloom
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/6431513
• 关键词: Carnivora; Parvoviridae; antibody formation; antiviral antibody; capsid; communicable disease diagnosis; cytokine; host organism interaction; immunoelectrophoresis; laboratory rabbit; microorganism culture; microorganism immunology; nucleic acid sequence; pathologic process; polymerase chain reaction; virus antigen; virus protein

Persistent infection of adult mink with the Aleutian mink disease parvovirus (ADV)leads to disturbances of immune regulation, including hypergammaglobulinemia, plasmacytosis, immune complex disease, interstitial and glomerulonephritis. Infection at the cellular level is noncytopathic and restricted. In contrast, infections in cell culture and in newborn mink are cytopathic and fully permissive. Studies in cell culture, using TUNEL labeling and annexin staining, have revealed that cells engaged in permissive ADV infection replication become apoptotic. Pretreatment of cells with a broad-spectrum caspase inhibitor or a specific inhibitor of the executioner caspase 3, blocks permissive replication at a step prior to viral protein expression. Treatment with an inhibitor specific for caspase 6/8 produces a partial block. Thus, ADV induces programmed cell death (apoptosis) and is in fact dependent upon apoptosis for complete viral replication. Populations of native feral mustelids in Spain are declining. The presence of ADV infection has been documented in these animals. More than 1 sequence variant of ADV appears to be circulating and these variants differ from previously identified isolates of ADV.

阿留申貂皮病细节病毒（ADV）对成年貂的持续感染会导致免疫调节的障碍，包括高γ-球蛋白血症，浆细胞增多症，浆细胞增多症，免疫复杂疾病，间质和肾小球肾炎。细胞水平的感染是无周到的和受限的。相反，细胞培养和新生貂皮中的感染是细胞疗法和完全允许的。使用TUNEL标记和膜联蛋白染色的细胞培养研究的研究表明，从事允许ADV感染复制的细胞变得凋亡。用广谱caspase抑制剂或execution子caspase 3的特定抑制剂对细胞进行预处理，在病毒蛋白表达前的一步中阻止允许的复制。用特异性胱天蛋白酶6/8的抑制剂治疗会产生部分阻滞。因此，ADV诱导了程序性细胞死亡（凋亡），实际上取决于凋亡的完全病毒复制。西班牙本地野性的本地野性种群正在下降。这些动物已经记录了ADV感染的存在。 ADV的1个以上序列变体似乎是在循环，这些变体与先前确定的ADV分离株有所不同。