Answers are grounded in this paper and cite their sources.
Mumps virus exhibits cardiotropism in vitro due to more efficient viral release in heart cells compared to lung and liver cells.
The cardiotropism of mumps virus in ovo was reproduced in vitro in a comparative study of the replication of mumps virus in cultivated heart, lung, and liver cells from 11-to 19-day-old chicken embryos. The increased proportion of virus-producing cells in the heart was shown not to be due to greater adsorption of virus to heart cells. Neither interferon nor other cellular inhibitory products were responsible for the lower level of production of virus by lung and liver cells. The proportion of cells producing virus in relation to the amount of virus adsorbed and the proportion of hemadsorbing cells that released infectious virus were greater in heart cells; this finding suggested more efficient viral release in the heart than at the other sites. Inhibition of protein synthesis by puromycin after infection rapidly stimulated the production of mumps virus only in liver cells. Thus a relatively late stage in viral synthesis may be attenuated in the less susceptible liver cells, and events late in viral synthesis may determine organ-related differences in the multiplication of mumps virus in ovo.
No takes yet. Share an insight, caveat, or question.
Davis et al. (1975) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: