Clem R J, Robson M, Miller L K
Department of Genetics, University of Georgia, Athens 30602.
J Virol. 1994 Oct;68(10):6759-62. doi: 10.1128/JVI.68.10.6759-6762.1994.
The infectivity of Autographa californica nuclear polyhedrosis virus mutants lacking the apoptosis-inhibiting gene p35 is decreased 1,000-fold or more in larvae of the insect Spodoptera frugiperda if the budded form of the virus is administered by hemocoelic injection; this decrease is correlated with the antiviral effects of apoptosis (R. J. Clem and L. K. Miller, J. Virol. 67:3730-3738, 1993). We have extended this correlation by showing that the infectivity of p35 mutant budded virus is restored to wild-type levels by expression of an unrelated baculovirus apoptosis-inhibiting gene, Cp-iap. We have also examined the oral infectivity of the occluded form of mutants lacking p35, the neighboring p94 gene, or both genes by feeding insects occluded virus. The oral infectivity of the p35 mutant was significantly reduced in S. frugiperda larvae, but this reduction (25-fold) was less than that observed for the hemocoelic route of infection (1,000-fold). The disruption of p94 alone had no apparent effect on infectivity by either route. Unexpectedly, however, the disruption of both p35 and p94 restored oral infectivity to nearly wild-type levels but did not exert this compensatory effect on infectivity by hemocoelic injection. Thus, the infectivity of the double p35/p94 mutant is affected in a route-specific manner in S. frugiperda larvae, suggesting a tissue-specific response to p35 and/or p94. Infectivity in a different host, Trichoplusia ni, was unaffected by all the mutants tested, consistent with previous studies indicating a lack of sensitivity to apoptosis in this species. However, T. ni and S. frugiperda larvae infected with p35 mutants failed to exhibit the symptom of morphological disintegration ("melting") typical of a wild-type infection, suggesting that p35 is required for the infection of some tissues in both species.
如果通过血腔注射给予苜蓿银纹夜蛾核型多角体病毒（Autographa californica nuclear polyhedrosis virus）缺失凋亡抑制基因p35的突变体的出芽形式，则其在草地贪夜蛾（Spodoptera frugiperda）幼虫中的感染力会降低1000倍或更多；这种降低与凋亡的抗病毒作用相关（R. J. 克莱姆和L. K. 米勒，《病毒学杂志》67:3730 - 3738, 1993）。我们通过证明表达一个不相关的杆状病毒凋亡抑制基因Cp-iap可将p35突变体出芽病毒的感染力恢复到野生型水平，扩展了这种相关性。我们还通过给昆虫喂食包涵体病毒，检测了缺失p35、相邻的p94基因或这两个基因的突变体的包涵体形式的口服感染力。p35突变体在草地贪夜蛾幼虫中的口服感染力显著降低，但这种降低（25倍）小于血腔感染途径所观察到的降低（1000倍）。单独破坏p94对两种途径的感染力均无明显影响。然而，出乎意料的是，破坏p35和p94两者可将口服感染力恢复到接近野生型水平，但对血腔注射的感染力没有这种补偿作用。因此，双p35/p94突变体的感染力在草地贪夜蛾幼虫中以途径特异性方式受到影响，这表明对p35和/或p94存在组织特异性反应。在另一种宿主粉纹夜蛾（Trichoplusia ni）中，所有测试的突变体均未影响其感染力，这与先前表明该物种对凋亡缺乏敏感性的研究一致。然而，感染p35突变体的粉纹夜蛾和草地贪夜蛾幼虫均未表现出野生型感染典型的形态解体（“融化”）症状，这表明p35是这两个物种中某些组织感染所必需的。
