Haller O, Arnheiter H, Lindenmann J
Infect Immun. 1976 Mar;13(3):844-54. doi: 10.1128/iai.13.3.844-854.1976.
Mice carrying the gene Mx were resistant to the lethal action of a hepatotropic line of avian influenza A virus. In resistant animals, foci of liver necrosis were self-limiting, and maximal virus titers reached were much below those in susceptible animals. Resistance could not be abrogated by immunosuppressive treatment with cyclophosphamide, methotrexate, or procarbazine, although such treatment prevented cellular infiltration at sites of virus replication and appeared to delay virus clearance. Silica and thorium dioxide, thought to inhibit macrophage function, likewise failed to abolish resistance. Regenerating liver tissue did not support more extensive virus replication than did intact adult liver.
携带Mx基因的小鼠对嗜肝性甲型禽流感病毒株的致死作用具有抗性。在抗性动物中,肝坏死灶是自限性的,达到的最大病毒滴度远低于易感动物。用环磷酰胺、甲氨蝶呤或丙卡巴肼进行免疫抑制治疗并不能消除抗性,尽管这种治疗可防止病毒复制部位的细胞浸润,且似乎会延迟病毒清除。二氧化硅和二氧化钍被认为可抑制巨噬细胞功能,但同样未能消除抗性。再生肝组织并不比完整的成年肝脏更能支持病毒的广泛复制。