由禽骨质疏松病毒的快速和慢发斑块分离株引起的骨质疏松的发病机制

R.E. Smith , J.H. Morgan ∗
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引用次数: 8

摘要

对感染了禽骨质疏松病毒分离株的10日龄胚胎鸡的骨骼进行检查发现,MAV-2(O)空斑分离株32/2/4可导致骨快速生长,而MAV-2(O)空斑分离株13可导致轻度骨生长。MAV-2(O)空斑分离物32/2/4注射到8日龄的小鸡体内可引起贫血,注射到4日龄的胚胎中可引起蛋内骨生长。在病毒感染后第1天,胚胎被给予抗体,被动给予中和抗体对mav2 (O)诱导的骨生长有保护作用。中和抗体对正常鸡和法氏囊切除鸡的急性贫血也有保护作用,但抗体不能预防法氏囊切除鸡的慢性贫血或骨质疏松的出现。MAV-2(O)缓慢发作的斑块分离物在动物体内反复传代,导致病毒逐渐诱导更严重的骨骼生长和贫血。
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Pathogenesis of osteopetrosis induced by rapid and slow onset plaque isolates of an avian osteopetrosis virus

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.

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Background review for the '2015 European guideline on the management of Chlamydia trachomatis infections'. Author index Keyword index Pathogenesis of osteopetrosis induced by rapid and slow onset plaque isolates of an avian osteopetrosis virus Dichloromethylene diphosphonate (Cl2MDP) reduces natural killer (NK) cell activity in mice
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