In the current issue of PLoS, German investigators Scrivano, et al. explore cytomegalovirus (CMV) in vitro infection of endothelial cells (EC) and fibroblasts. Currently, little is known about CMV cell entry and receptor binding. The putative candidates, glyoproteins gH/gL promote membrane fusion and the formation of either gH/gL/gO or gH/gL/pUL complexes. Where laboratory strains express the prior, live virions have been observed to incorporate the latter. In changing the surface protein content/expression, this consequently alters the ability of the virus to infect certain cell types. Where the lab strain is restricted to only fibroblasts and neuronal cells, the gH/gL/pUL strain can infect leukocytes, dendritic , epithelial and endothelial cells.
This paper examines the resultant progeny from various cell type infections and determinants of cell tropism. Using an SV40 promoter-driven luciferase expression cassette with mutant inserts and differential cell entry/infection assays, they determine that infection capacities are determined by either EC-tropic or non-EC tropic virus populations. Ultimately, this is a reflection on the producer host cell of CMV that directs the infection. They go on to propose a CMV model wherein the production of a heterogeneous virus progeny from fibroblasts and EC is directed by pUL128--pUL128 progeny, whereas EC release a non EC-tropic pUL128 progeny and retain the EC-tropic virus. This results in a switch of the spread mode from supernatant-based (gO) to focal driven(gP).
Scrivano L, Sinzger C, Nitschko H, Koszinowski UH, Adler B (2011) HCMV Spread and Cell Tropism are Determined by Distinct Virus Populations. PLoS Pathog 7(1): e1001256. doi:10.1371/journal.ppat.1001256