Two clinical isolates and the toledo strain of cytomegalovirus contain endothelial cell tropic variants that are not present in the AD169, Towne, or Davis strains
Lp. Maccormac et Je. Grundy, Two clinical isolates and the toledo strain of cytomegalovirus contain endothelial cell tropic variants that are not present in the AD169, Towne, or Davis strains, J MED VIROL, 57(3), 1999, pp. 298-307
The highly fibroblast-passaged AD169, Towne, and Davis strains of cytomegal
ovirus (CMV) were found to have a restricted capacity to infect endothelial
cells in vitro. Although such replication could be increased by a combinat
ion of low speed centrifugation and sodium butyrate treatment, the extracel
lular virus produced was infectious for fibroblasts but not for endothelial
cells. In contrast, the low passage Toledo strain, and a low passage fibro
blast-grown clinical isolate of CMV, C1F, could be continually passaged in
endothelial cells, giving the strains C1FE and Toledo.E. Whilst, using the
conditions described above, initial infection of endothelial cells with AD1
69 or C1F resulted in similar titres of extracellular virus as assayed on f
ibroblasts, only the virus from the C1F strain was infectious for endotheli
al cells. Passage of C1F in fibroblasts decreased its ability to infect end
othelial cells, whilst retaining equal ability to infect fibroblasts. Altho
ugh endothelial-cell-passaged cell-free C1FE virus was endothelial cell-tro
pic, it was still much more infectious for fibroblasts than for endothelial
cells. It is concluded that the C1F and Toledo strains, but not the AD169,
Towne, or Davis strains, contained endothelial cell tropic variants, which
could be lost on passage through fibroblasts, but retained on passage thro
ugh endothelial cells. Furthermore, virus in an ex vivo source of CMV, a bl
ood specimen, was found to be more tropic for fibroblasts than for endothel
ial cells, suggesting that in vivo CMV exists as quasi strains with differe
nt cell tropism, some of which might be lost in vitro by passage in an inap
propriate cell type. J. Med. Virol. 57:298-307, 1999. (C) 1999 Wiley-Liss,
Inc.