ExtractGrowth retardation in the mumps virus-infected chicken model is not due to a reduction in cell number but appears to Embryonic mumps virus infection in the avian host leads to be caused by a diminution in cell size. fetal growth retardation. The mechanism of this retardation has not been established.The avian host is unique in that the direct effect of a virus Speculation On the may be ascertained in the absence of a The relation between embryonic mumps virus infection and placenta.myocarditis is supported by the findings of high titers of virus Using radioisotope labeling techniques, RNA, and throughout the incubation period. It is postulated that altered protein metabolism was investigated in tissues from infected cardiac function results in a state of hypofusion and a and control chickens. Metabolism in organ tissue cultivated in preferential effect is seen in the brain with consequent vitro and then infected was also studied using the same diminution of cell size rather than cell radioisotope techniques.At hatch, the mean body weight of eight experimental chickens infected with mumps virus early during embryonic incubation was significantly less than that of 19 controls. This lower weight was evident in the brain of the infected chickens. The brain and carcass contained decreased amounts of RNA and protein when compared with uninfected control chickens. The kidney was the only other organ in which the protein content in experimental chickens was less than in controls.There was no difference in the DNA content of organs from in ovo-infected and control chickens or organ tissues cultivated in vitro before infection with mumps virus. Similarly, measurements of cell number at the same time were equal. Viral assay of the chickens infected in ovo revealed highest titers of virus in the heart throughout the last half of incubation. Intermediate titers of virus were recovered from 'the lung, spleen, and skeletal muscle. Low quantities of virus were recovered from the brain and liver. The bursa contained high titers of virus at midincubatio~ but these titers rapidly declined by hatch.Embryonic growth retardation has been attributed to many factors, including metabolic defects (lo), malnutrition of fetal and maternal origin (20, 24, 25, 32), congenital anomalies (3, 21), and infection (1,2,26). Under normal conditions the embryo grows as the population and size of cells increase. Conditions which impair either cellular variable will result in growth retardation. Several experimental models of fetal growth retardation in the mammal have been particularly illuminating. Wigglesworth (3 1 ) and Emmanouilides e t al. (9) ligated the uterine and umbilical arteries of the rat and sheep, respectively, producing placental insufficiency which resulted in fetal growth retardation.The avian model offers the opportunity for unique experimentation in that the direct effect of a virus on the chicken embryo may be ascertained in the absence of a placenta. Previous work has demonstrated that mumps virus infection during early ...