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禽骨质石化病毒快速和缓慢发病斑块分离株诱导的骨质石化的发病机制

Pathogenesis of osteopetrosis induced by rapid and slow onset plaque isolates of an avian osteopetrosis virus.

作者信息

Smith R E, Morgan J H

出版信息

Metab Bone Dis Relat Res. 1984;5(6):289-98. doi: 10.1016/0221-8747(84)90016-x.

Abstract

Examination of bone from chickens infected as 10-day-old embryos with isolates of an avian osteopetrosis virus revealed that MAV-2(O) plaque isolate 32/2/4 caused rapid bone growth, while MAV-2(O) plaque isolate 13 caused a mild form of bone growth. MAV-2(O) plaque isolate 32/2/4 caused anemia when injected into the 8-day-old hatched chick and bone growth in ovo when injected into the 4-day-old embryo. Passive administration of neutralizing antibody protected against MAV-2(O)-induced bone growth when antibody was given to the embryo 1 day after virus. Neutralizing antibody also protected against an acute anemia observed when normal and bursectomized chickens were given MAV-2(O) 32/2/4, but antibody did not prevent the appearance of a chronic anemia or osteopetrosis in bursectomized chickens. Repeated animal passage of a slow onset plaque isolate of MAV-2(O) caused the virus to progressively induce more severe bone growth and anemia.

摘要

对10日龄胚胎感染禽骨质石化病毒分离株的鸡的骨骼进行检查发现,MAV - 2(O)蚀斑分离株32/2/4导致骨骼快速生长,而MAV - 2(O)蚀斑分离株13引起轻度骨骼生长。MAV - 2(O)蚀斑分离株32/2/4注射到8日龄出壳雏鸡时会导致贫血,注射到4日龄胚胎时会导致胚胎内骨骼生长。当在病毒感染后1天给胚胎注射中和抗体时,被动给予中和抗体可预防MAV - 2(O)诱导的骨骼生长。当正常鸡和法氏囊切除鸡接种MAV - 2(O) 32/2/4时,中和抗体还可预防观察到的急性贫血,但抗体不能防止法氏囊切除鸡出现慢性贫血或骨质石化。MAV - 2(O)的一种慢发蚀斑分离株经动物多次传代后,该病毒逐渐诱导出更严重的骨骼生长和贫血。

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