Matteucci D, Toniolo A, Conaldi P G, Basolo F, Gori Z, Bendinelli M
J Infect Dis. 1985 Jun;151(6):1100-8. doi: 10.1093/infdis/151.6.1100.
Adult mice infected with coxsackievirus B3 (CB3) showed a generalized lymphoid involution. This effect was produced by most of the isolates and clones of CB3 and, to a lesser extent, by coxsackievirus B1 but not by other highly pathogenic picornaviruses. While moderate involution of the thymus also occurred in mild CB3 infections, peripheral changes strictly correlated with the severity of disease. The major alteration of the thymus was a massive cortical depletion, whereas the reduction of spleen and lymph node cellularity appeared devoid of selectivity. No histological and ultrastructural signs of CB3 replication in such organs could be detected. Attempts to demonstrate CB3 replication in thymus, spleen, and lymph node cells were unsuccessful. CB3-induced lymphoid atrophy was not prevented by adrenalectomy and was exacerbated by three different immunopotentiating agents. Thus, certain picornaviruses may cause severe stress-independent lymphoid damage in the absence of viral replication in situ. A role for autoreactive mechanisms is suggested.
感染柯萨奇病毒B3（CB3）的成年小鼠出现全身性淋巴组织退化。这种效应是由大多数CB3分离株和克隆株产生的，在较小程度上由柯萨奇病毒B1产生，但其他高致病性微小核糖核酸病毒则不会产生这种效应。虽然在轻度CB3感染中胸腺也会发生中度退化，但外周变化与疾病严重程度严格相关。胸腺的主要改变是皮质大量耗竭，而脾脏和淋巴结细胞数量的减少似乎没有选择性。在这些器官中未检测到CB3复制的组织学和超微结构迹象。在胸腺、脾脏和淋巴结细胞中证明CB3复制的尝试均未成功。肾上腺切除术并不能阻止CB3诱导的淋巴组织萎缩，三种不同的免疫增强剂会使其加剧。因此，某些微小核糖核酸病毒可能在原位没有病毒复制的情况下导致严重的、与应激无关的淋巴组织损伤。提示存在自身反应机制。
