Greenberg H, Helms C M, Brunner H, Chanock R M
Proc Natl Acad Sci U S A. 1974 Oct;71(10):4015-9. doi: 10.1073/pnas.71.10.4015.
Temperature sensitive mutants of Mycoplasma pneumoniae were developed with the expectation that their temperature sensitive defects would restrict replication in vivo at the temperature of the lower respiratory tract, whereas such defects would not seriously impair replication in the cooler environment of the upper respiratory passages. One such ts mutant, ts-H43, which does not replicate at a temperature of 37 degrees or above, although noninfectious for hamsters, infected each of 16 seronegative adult volunteers when given by the intranasal route. The mutant remained genetically stable throughout the course of infection and stimulated a moderate systemic and local antibody response. The mutant was entirely avirulent for the volunteers but appeared to stimulate resistance to subsequent challenge with partially attenuated wild-type (ts(+)) Mycoplasma pneumoniae.
其温度敏感缺陷会限制在下呼吸道温度下的体内复制,而在温度较低的上呼吸道环境中,此类缺陷不会严重损害复制。一种这样的温度敏感突变体ts-H43,在37度及以上温度时不复制,虽然对仓鼠无感染性,但经鼻内途径给予时,感染了16名血清阴性的成年志愿者中的每一个。该突变体在整个感染过程中保持基因稳定,并激发了适度的全身和局部抗体反应。该突变体对志愿者完全无毒,但似乎刺激了对随后部分减毒的野生型(ts(+))肺炎支原体攻击的抵抗力。