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鼠巨细胞病毒感染中的心肌心包炎和增强的营养不良性心脏钙化

Myopericarditis and enhanced dystrophic cardiac calcification in murine cytomegalovirus infection.

作者信息

Gang D L, Barrett L V, Wilson E J, Rubin R H, Medearis D N

出版信息

Am J Pathol. 1986 Aug;124(2):207-15.

Abstract

In mice inoculated with murine cytomegalovirus (MCMV) an acute myopericarditis developed which varied from a focal lymphohistiocytic inflammation to intense inflammation with necrosis and cytomegalic inclusion-bearing cells. Sublethal doses caused focal transient nonspecific chronic inflammation, followed months later by an increased frequency and extent of dystrophic cardiac calcification. When such latently infected hearts were heterotopically transplanted into uninfected animals which were then immunosuppressed (IS), a fatal generalized CMV infection followed. Cytomegalic inclusion-bearing endothelial, fibroblastic, and myocardial cells were seen in the intense inflammation found in hearts taken from mice 4 days after lethal inoculation and transplanted into uninfected mice, which were then IS. These findings may be relevant to human cardiac transplantation because they show that MCMV regularly causes cardiac infection with both acute and chronic consequences; chronic injury may follow a morphologically nonspecific myopericarditis which might not be attributed to CMV infection.

摘要

在接种了鼠巨细胞病毒(MCMV)的小鼠中,会发生急性心肌心包炎,其表现从局灶性淋巴细胞组织细胞炎症到伴有坏死和含巨细胞包涵体细胞的严重炎症不等。亚致死剂量会导致局灶性短暂非特异性慢性炎症,数月后营养不良性心脏钙化的频率和范围增加。当将这种潜伏感染的心脏异位移植到未感染的动物体内,然后对这些动物进行免疫抑制(IS)时,会发生致命的全身性CMV感染。在致死接种4天后从小鼠取出并移植到未感染小鼠(然后进行免疫抑制)的心脏中发现的严重炎症中,可见含巨细胞包涵体的内皮细胞、成纤维细胞和心肌细胞。这些发现可能与人类心脏移植有关,因为它们表明MCMV经常导致心脏感染,并产生急性和慢性后果;慢性损伤可能继发于形态学上非特异性的心肌心包炎,而这种炎症可能不归因于CMV感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27f2/1888281/f2f3d4af2f2e/amjpathol00155-0038-a.jpg

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