Biomedical subjects

H S GINSBERG

Publications and source records attributed to H S GINSBERG.

65 records · Page 4Linked to original sources

PubMed1951

The dependence of the pathological lesion upon the multiplication of pneumonia virus of mice (PVM); kinetic relation between the degree of viral multiplication and the extent of pneumonia.

The rate of multiplication of PVM in the mouse lung is relatively constant, averaging 7.9-fold per day with but slight variations, irrespective of the amount of virus inoculated. Similarly, the rate of increase in the amount of pneumonia is relatively constant, averaging 4.7-fold per day, even though the quantity of virus inoculated is varied over a wide range. It follows that viral multiplication proceeds 1.7 times more rapidly than does extension of the pathological lesion, both reaching limiting maximal values in periods which are predictable from the amount of virus inoculated. From the concentration of virus determined at any time during the incremental period, the amount of pneumonia present earlier or later in the incremental period can be computed with considerable precision. The results support the postulate that the extent of the pathological lesion is dependent upon the degree of viral multiplication.

Animals↗

PubMed1951

Characteristics of the multiplication cycle of pneumonia virus of mice (PVM).

A study of the multiplication of PVM in the mouse lung yielded evidence in support of the hypothesis that discrete cycles occur. The cycle is characterized by a latent period of about 15 hours, an incremental period of 10 to 15 hours and a total duration of 24 to 30 hours. The yield of virus per cycle is approximately 16-fold. A large proportion, approximately 90 per cent, of PVM is lost on intranasal inoculation and cannot be recovered from the lung. Of the virus which reaches the lung, almost all becomes non-infective within 12 hours even though a considerable amount retains the capacity to cause hemagglutination. During the incremental period infective virus appears as soon as any increase in hemagglutination is demonstrable.

Animals↗

PubMed1951

Therapy of infection with pneumonia virus of mice (PVM); effect of a polysaccharide on the multiplication cycles of the virus and on the course of the viral pneumonia.

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.

Animals↗

PubMed1951

Mechanism of production of pulmonary lesions in mice by Newcastle disease virus (NDV).

Infectious NDV particles produce extensive pulmonary consolidation in the mouse in the absence of demonstrable virus multiplication. The lesions are indistinguishable from those of influenza A virus infection. This effect of NDV was blocked by intranasal injection of RDE or immune serum before virus inoculation, but not by immune serum injected 5 minutes or more after NDV. Influenza A virus infection did not diminish fixation of NDV in excised lungs but did interfere with the injurious action of this agent in the living mouse. The analogy between these reactions and those which take place in a progressive virus infection is pointed out, and the mechanism of production of lesions in virus pneumonias discussed.

Animals↗

PubMed1951