The Journal of Experimental Medicine, Vol 93, 247-266,
Copyright, 1951, by The Rockefeller Institute for Medical Research New York
PATHOGENESIS OF COXSACKIE VIRUS INFECTION
:
MULTIPLICATION OF VIRUS AND EVOLUTION OF THE MUSCLE LESION IN MICE
Joseph L. Melnick Ph.D.1 and
Gabriel C. Godman M.D.1
1 From the Section of Preventive Medicine and Department of Pathology, Yale University School of Medicine, New Haven
The quantitative distribution of the Conn.-5 strain of Coxsackie virus in different tissues was determined by serial titration at intervals after inoculation of 4 to 5 day old mice. High titers were reached by the 2nd day in blood, heart, liver, muscle, intestine, and its contents, and these were maintained through the 8th day, except for the blood, in which the virus level fell earlier. In paralyzed mice, muscle and brain attained the highest titers and it was in these tissues alone that virus persisted through the 9th day of illness.
The pathology of the infection has been briefly described. In particular, the evolution of morbid changes in striated muscle was correlated with the concentrations of virus in muscle. Acute muscle necrosis first occurred when there was a peak viral concentration (4th day), and reached maximal intensity on the 8th day. Scattered acute lesions continued to appear while the virus titer remained above 10–4, from the 9th to 12th day. With the decrease in the myositis, there was a concomitant decrease in the incidence of perceptible disease. Inflammation was found to follow upon the development of necrosis, and subsided slowly. Regeneration began very early, became exuberant, and led finally to restitution of the muscle.
Submitted on November 1, 1950
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