Tanaka J, Ogura H, Fukuda S, Hatano M
Microbiol Immunol. 1978;22(12):765-73. doi: 10.1111/j.1348-0421.1978.tb00430.x.
The formation of cowpox virus-specific cell surface antigen (CPV S-ag) was significantly enhanced by double infection with HVJ (Sendai virus). Simultaneous double infection, superinfection with HVJ and superinfection with CPV of cells persistently infected with HVJ similarly enhanced the formation of CPV S-ag, while pre-infection with HVJ was ineffective. To be effective, cells must be infected at a m.o.i. of greater than or equal to 1.0 and HVJ gene functions had to be expressed. The HVJ-infected cell extracts had an ability to accelerate uncoating (or degradation) of CPV, causing an early increase and a subsequent decrease in the infectivity of CPV. This activity reached a maximum 4--6 hr after HVJ infection, the increase paralleling enhancement of the total activity of several cellular enzymes. Addition of puromycin abolished the increase of these activities and the formation of CPV S-ag. Thus, the double infection with HVJ of CPV-infected cells induces an enhancement of CPV S-ag formation presumably as a consequence of activation of cellular enzymes which in turn accelerates uncoating of CPV.
用HVJ(仙台病毒)双重感染可显著增强牛痘病毒特异性细胞表面抗原(CPV S-ag)的形成。同时双重感染、用HVJ进行超感染以及用CPV对持续感染HVJ的细胞进行超感染,同样能增强CPV S-ag的形成,而用HVJ进行预感染则无效。要产生效果,细胞必须以大于或等于1.0的感染复数进行感染,并且必须表达HVJ基因功能。感染HVJ的细胞提取物具有加速CPV脱壳(或降解)的能力,导致CPV感染力先增加后下降。这种活性在HVJ感染后4 - 6小时达到最大值,其增加与几种细胞酶总活性的增强平行。加入嘌呤霉素可消除这些活性的增加以及CPV S-ag的形成。因此,CPV感染细胞与HVJ双重感染可能通过激活细胞酶,进而加速CPV脱壳,从而诱导CPV S-ag形成增强。