Mandelli G, Rampin T, Finazzi M
Vet Pathol. 1978 Jul;15(4):531-43. doi: 10.1177/030098587801500411.
The avian reovirus "UM 1-203" originally isolated in the United States from chickens with tenosynovitis was pathogenic for the newborn chick infected by parenteral inoculation. It induced plurivisceral lesions, which became particularly intense in the liver. The intense local multiplication of the virus provoked a necrotizing hepatitis; viral titers were maintained around an E.I.D.50 of 10(8)/0.2 ml of organ suspension in chicks killed between the 3rd and 5th days after inoculation. As a specific cellular response to the viral multiplication, numerous polykaryocytes formed and increased in number, then regressed and disappeared from the hepatic parenchyma. By histologic and electron microscopic examination at progressive times after infection, the virus was recognizable in the polykaryocyte cytoplasm. In chicks that survived longer (killed the 5th and 6th days after inoculation), regeneration of the hepatic parenchyma occurred and seemed to develop from groups of dense hepatocytes that either lacked the virus or survived the acute phase of infection.
禽呼肠孤病毒“UM 1-203”最初于美国从患有腱鞘炎的鸡中分离得到，经肠胃外接种可感染新生雏鸡并使其致病。它会引发多脏器损伤，其中肝脏的损伤尤为严重。病毒在局部大量增殖，引发坏死性肝炎；在接种后第3天至第5天处死的雏鸡中，器官悬液的病毒滴度维持在约10(8)/0.2 ml的E.I.D.50左右。作为对病毒增殖的一种特异性细胞反应，大量多核细胞形成并增多，随后消退并从肝实质中消失。通过在感染后的不同时间进行组织学和电子显微镜检查，可在多核细胞的细胞质中识别出病毒。在存活时间较长的雏鸡（接种后第5天和第6天处死）中，肝实质发生再生，似乎是由缺乏病毒或在感染急性期存活下来的密集肝细胞群发展而来。
