Olson G B, Dent P B, Rawls W E, South M A, Montgomery J R, Melnick J L, Good R A
J Exp Med. 1968 Jul 1;128(1):47-68. doi: 10.1084/jem.128.1.47.
In vitro rubella virus infections of lymphocytes from normal adult humans impaired their responsiveness to phytohemagglutinin (PHA) stimulations; a situation which seemed analogous to the PHA unresponsiveness of peripheral lymphocytes from babies with the congenital rubella syndrome. Such in vitro viral infection of normal cells also decreased the synthesis of normal nucleic acids and structural proteins, and abrogated the enhanced DNA synthesis induced by pokeweed and specific antigen stimulations. Furthermore, it was shown that live rubella virus, but not ultraviolet-irradiated virus, was necessary for the impaired mitogenic responses of normal leukocytes. These observations are interpreted to favor the view that the virus achieves its inhibitory effect on the action of mitogens by interference either directly or indirectly at an intracellular site. Such an action could reduce the functional potential of lymphocytes and impair their effectiveness as immunologically competent cells or as effectors in immunologic reactions.
来自正常成年人的淋巴细胞在体外受到风疹病毒感染后，其对植物血凝素（PHA）刺激的反应能力受损；这种情况似乎类似于先天性风疹综合征婴儿外周淋巴细胞对PHA无反应的情况。正常细胞的这种体外病毒感染还会减少正常核酸和结构蛋白的合成，并消除由商陆和特异性抗原刺激诱导的DNA合成增强。此外，研究表明，活风疹病毒而非紫外线照射的病毒，是正常白细胞促有丝分裂反应受损所必需的。这些观察结果被解释为支持这样一种观点，即病毒通过直接或间接干扰细胞内位点来实现其对有丝分裂原作用的抑制作用。这种作用可能会降低淋巴细胞的功能潜力，并损害它们作为免疫活性细胞或免疫反应效应细胞的有效性。
