Gauntt C J, Jones D C, Huntington H W, Arizpe H M, Gudvangen R J, DeShambo R M
J Med Virol. 1984;14(4):341-55. doi: 10.1002/jmv.1890140407.
Neonatal or 7-day-old mice inoculated intracranially with either of two temperature-sensitive mutants (ts1, ts6) or the parent coxsackievirus B3 (CVB3) subsequently developed porencephaly or hydranencephaly. The forebrain anomaly induced depended upon age of the animal at inoculation and virus variant inoculated. Sections of brains from hydranencephalic mice revealed severe meningeal reactions, necrotizing encephalitis, and liquifactive necrosis in the cerebrum. No pathology was found in the pons, medulla, or cerebellum. Immunofluorescence studies with hyperimmune anti-CVB3 antiserum showed a random distribution of virus-infected cells in the cerebrum. Virus was recovered from several organs but little to no interferon and no anti-CVB3 neutralizing antibody were present in brain tissues. Availability of cells for replication of virus at the time of inoculation and replicative properties of each virus likely contributed to the outcome. Thus, forebrain anomalies resembling those found in infants can be induced in a murine model by select variants of coxsackievirus B3.
用两种温度敏感突变体（ts1、ts6）或亲代柯萨奇病毒B3（CVB3）中的任何一种经颅内接种新生小鼠或7日龄小鼠后，随后会出现孔洞脑或积水性无脑畸形。所诱导的前脑异常取决于接种时动物的年龄以及接种的病毒变体。积水性无脑畸形小鼠的脑切片显示脑膜有严重反应、坏死性脑炎以及大脑中的液化性坏死。脑桥、延髓或小脑未发现病理变化。用超免疫抗CVB3抗血清进行的免疫荧光研究显示，大脑中病毒感染细胞呈随机分布。病毒从多个器官中检出，但脑组织中几乎没有或没有干扰素，也没有抗CVB3中和抗体。接种时病毒复制可用细胞的可用性以及每种病毒的复制特性可能促成了这一结果。因此，柯萨奇病毒B3的特定变体可在小鼠模型中诱导出类似于婴儿中发现的前脑异常。
