Khan N C, Poddar R K
J Virol. 1974 May;13(5):997-1000. doi: 10.1128/JVI.13.5.997-1000.1974.
Bacteriophage phiX174 when photodynamically inactivated (i.e., when rendered unable to produce plaques as a result of exposure to visible light in air in the presence of proflavine) progressively lost their capacity to bind efficiently with homologous antiserum. Such loss of serum-blocking power was evident with heat-inactivated but not with UV-irradiated phage. The ability of the phages to adsorb to host cells, however, remained practically unaltered even after photodynamic inactivation. It thus appears that photodynamic damages in the so-called "jacket" component of the phiX174 coat proteins are partly responsible for the loss of plaque-forming ability, whereas the "spikes" are either poor antigens or insensitive to photodynamic treatment.
噬菌体phiX174在光动力失活时(即由于在空气中、黄素存在的情况下暴露于可见光而无法产生噬菌斑时),与同源抗血清有效结合的能力逐渐丧失。这种血清阻断能力的丧失在热灭活的噬菌体中很明显,但在紫外线照射的噬菌体中则不明显。然而,即使经过光动力失活,噬菌体吸附宿主细胞的能力实际上仍未改变。因此,看来phiX174外壳蛋白所谓“衣壳”成分中的光动力损伤部分导致了噬菌斑形成能力的丧失,而“刺突”要么是弱抗原,要么对光动力处理不敏感。