Gómez R M, Lascano E F, Berría M I
Departamento de Microbiología, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
J Med Virol. 1991 Oct;35(2):71-5. doi: 10.1002/jmv.1890350202.
Balb/C weanling mice were inoculated intraperitoneally with a myocarditic variant of coxsackie-virus B3, with the aim of characterizing more fully the cell damage induced in the heart as well as in other organs. During the first week postinfection (pi), all animals developed acinar pancreatitis, followed by focal myocarditis. In accordance with the increasing infectivity titers, such progressive histopathological changes correlated with local viral replication. From day 4 pi, acinar degeneration accompanied by diffuse inflammatory exudate was observed in the pancreas, followed by fatty tissue replacement by day 8. In the heart, focal necrosis rather than inflammatory reaction first appeared at 4 days pi and became widespread by 6-8 days pi. Necrotic foci usually presented calcium deposits, with absence of myofibrils in the affected fibers. The fact that both periodic acid Schiff (PAS) and Best carmine staining remained positive even after diastase treatment ruled out basophilic necrosis. In summary, the pancreas appeared to be the site of primary viral replication leading to viremia.
将Balb/C断奶小鼠通过腹腔注射接种柯萨奇病毒B3的心肌炎变种,目的是更全面地表征心脏以及其他器官中诱导的细胞损伤。在感染后(pi)的第一周,所有动物均发生腺泡性胰腺炎,随后出现局灶性心肌炎。随着感染性滴度的增加,这种进行性组织病理学变化与局部病毒复制相关。从感染后第4天开始,在胰腺中观察到腺泡变性并伴有弥漫性炎性渗出物,到第8天被脂肪组织替代。在心脏中,局灶性坏死而非炎症反应在感染后第4天首次出现,并在感染后6 - 8天广泛扩散。坏死灶通常呈现钙沉积,受影响的纤维中无肌原纤维。即使在淀粉酶处理后,过碘酸希夫(PAS)染色和贝斯特胭脂红染色仍呈阳性,这一事实排除了嗜碱性坏死。总之,胰腺似乎是导致病毒血症的原发性病毒复制部位。