Visceral pathology of acute systemic injury in newborn mice on the onset of Coxsackie virus infection.

Coxsackievirus B (CVB) is a significant pathogen of neonatal diseases with severe systemic involvement and high mortality. Hence, it is essential to develop a CVB-induced acute systemic disease model on newborn mouse and study the injury at the onset phase. In this work, a clinical strain of CVB3, Nancy, and its variant strain, Macocy, were adopted in 24 hour old neonates by oral infection. The pathological changes in the heart, liver and lung tissues were analyzed by pathology assays. In situ end labeling assay for programmed cell death was carried out for liver tissues. The data on fatality and infection rates and pathology scores were analyzed statistically. The genomic sequences of the two strains were aligned. The model represented the manifest clinical syndromes of hepatitis, pneumonia and myocardial injury at the onset phase, in which massive numbers of hepatocytes had undergone programmed cell death. Statistical and pathological analysis indicated that the myocardial injury was mild, whereas the liver and lung were more severe. The fatality rate, infection and pathology of the two CVB strains were the same. Therefore, two nucleotide mutations in the 5' UTR and four amino acid mutations in polyprotein, which did not alter virulence, were shown. By peroral CVB infection of neonatal mice, we developed an acute systemic disease model for studying visceral pathology and systemic disease. At the onset of acute neonatal systemic disease, the hepatitis and pneumonia may be the dominant reason of death, as the injury of liver and lung is more severe than that of heart.