GINSBERG H S, HORSFALL F L
J Exp Med. 1951 Feb;93(2):161-71. doi: 10.1084/jem.93.2.161.
Inhibition of the multiplication of PVM by the capsular polysaccharide of Friedländer bacillus, type B, is associated with restriction in the development of pneumonia induced with the virus in the mouse lung. The extent of the pneumonic process appears to be a function of the degree of viral multiplication; the greater the inhibition of multiplication, the less extensive is the pneumonia and the more probable is the recovery of animals treated with the polysaccharide. Effective therapy of pneumonia induced in mice with PVM is obtained with a single injection of 0.02 mg. of the substance given intranasally either 2 or 3 days after inoculation. Under appropriate conditions, treated animals recover completely from a viral infection which is, in control animals, uniformly fatal. The polysaccharide produces inhibition if given in the first two-thirds of the latent period of the multiplication cycle, i.e., within 10 hours, but is ineffective when given at 12 hours or later. However, the second cycle and subsequent cycles are inhibited irrespective of the time the substance is injected during the first cycle of multiplication. The findings are discussed in relation to a theory regarding the mechanism of action of the polysaccharide.
B型弗里德兰德杆菌的荚膜多糖对肺炎病毒(PVM)增殖的抑制作用,与小鼠肺部该病毒诱发的肺炎发展受限有关。肺炎病变的程度似乎是病毒增殖程度的函数;增殖抑制程度越大,肺炎范围越小,接受多糖治疗的动物恢复的可能性就越大。在接种后2天或3天经鼻内单次注射0.02毫克该物质,可有效治疗小鼠由PVM诱发的肺炎。在适当条件下,接受治疗的动物能从病毒感染中完全康复,而在对照动物中,这种感染通常是致命的。如果在增殖周期潜伏期的前三分之二内(即10小时内)给予多糖,它会产生抑制作用,但在12小时或更晚给予则无效。然而,无论在第一个增殖周期中何时注射该物质,第二个周期及后续周期都会受到抑制。结合多糖作用机制的理论对这些发现进行了讨论。