Okada H, Okada N
Immunology. 1981 Jun;43(2):337-44.
HeLa cells infected with Sendai virus (SV) acquired the ability to activate the alternative pathway (AP) of guinea-pig complement without antibody reaction. For induction of complement activating ability (CAA), at least 2 hr incubation of the infected cells was required. However, ultraviolet (UV)-irradiation (8400 erg/mm2) of SV did not impair the inducibility of CAA and 51Cr-labelled HeLa cells infected with UV-irradiated SV (UV-SV) became readily cytolysed by C4-deficient guinea-pig complement without antigen-antibody reaction. This phenomenon may represent a primary in vivo defence mechanism against SV infection by eliminating the virus-infected cells via activation of complement on the cell surface. Although SV-infected HeLa cells activated the AP of guinea-pig complement, they did not activate the AP of human or mouse complement. The species restriction in the CAA induced by SV infection may result in different pathological manifestations in virus-infected animals and may affect their susceptibility to this type of infection.
感染仙台病毒（SV）的HeLa细胞获得了在无抗体反应情况下激活豚鼠补体替代途径（AP）的能力。为诱导补体激活能力（CAA），感染细胞至少需要孵育2小时。然而，用紫外线（UV）照射（8400尔格/平方毫米）的SV并不损害CAA的诱导能力，用UV照射的SV（UV-SV）感染的51Cr标记的HeLa细胞在无抗原-抗体反应的情况下很容易被C4缺陷的豚鼠补体溶解。这种现象可能代表了一种主要的体内防御机制，通过在细胞表面激活补体来消除病毒感染的细胞，从而抵御SV感染。尽管感染SV的HeLa细胞激活了豚鼠补体的AP，但它们并未激活人或小鼠补体的AP。SV感染诱导的CAA中的物种限制可能导致病毒感染动物出现不同的病理表现，并可能影响它们对这种感染类型的易感性。
